Schisandra B inhibits proliferation, migration and invasion of bladder cancer by regulating the Wnt/β‑catenin signaling pathway

Objective:To investigate the effects of Schisandra B on proliferation,migration,invasion of bladder cancer and to further investigate its molecular mechanism.Methods:Bladder cancer cells were subjected to different concentrations of Schisandra B solution(0,20,40,80μmol/L).CCK-8 assay was used to detect the effect of schisandra B on bladder cancer cell proliferation.Transwell migration assay and wound healing assay were used to detect the effect of Schisandra B on the migration of bladder cancer cells.Transwell invasion assay was used to detect the effect of schisandra B on invasion ability of bladder cancer cells.The expression levels of intracellularβ-catenin and c-myc protein were measured by western blot.Results:Schisandra B inhibited the proliferation of T24 and UM-UC-3 cells in a concentration and time dependent manner(P<0.05).The rate of wound healing and number of migration and invasion cells decreased with the increase of Schisandra B concentration(P<0.05).The expression ofβ-catenin and c-myc decreased after treatment with Schisandra B in bladder cancer cells(P<0.05).Conclusion:Schisandra B can inhibit the proliferation,migration and invasion of human bladder cancer T24 and UM-UC-3 cells,and the main mechanism for its inhibitory effect may be related to the inactivation of the Wnt/β-catenin signaling pathway.

Effect of Cx32 over‑expression on cell proliferation, migration, and invasion of hepatocellular carcinoma cell line Huh7 and its mechanism

Objective: To explore the effect of connexin 32 (Cx32) on the cell proliferation, migration, invasion of human hepatocellular carcinoma (HCC) cell line Huh7 and its mechanism. Methods: Firstly, bioinformatics techniques were used to analyze the difference in expression of Cx32 between HCC tissues and normal liver tissues, and the relationship between Cx32 expression and important clinicopathological features of HCC was also explored. Subsequently, Cx32 expression in HCC cell lines and normal hepatic epithelial cell line was detected in vitro. Huh7 cell line with stable over⁃expression of Cx32 was further established, and the change in cell proliferation ability was measured by MTT assay, changes in migration and invasion capacities were detected by wound⁃healing assay and transwell assay, on this cell line. Finally, western blot and immunofluorescence (IF) were used to investigate the alterations of expression of epithelial⁃mesenchymal transition (EMT) markers. Results: Bioinformatics analyses showed that Cx32 mRNA and protein expression levels in HCC tissues were lower than those in normal liver tissues, and the mRNA expression level of Cx32 was negatively correlated with T stage, histological grade and clinical stage of HCC patients (all P<0.05). Results of in vitro experiments revealed Cx32 protein expression in different HCC cell lines was down⁃regulated compared to that in normal hepatic epithelial cell line LO2. Cx32 stably over⁃expressed (Cx32 OE) Huh7 cell line was successfully constructed by lentivirus infection and showed high expression of Cx32 protein in the cell line. Compared to the control group and (or) the negative control (NC) group, the Cx32 OE group exhibited decreased OD490 value, wound healing rate and invasive cell number (all P<0.05). Furthermore, an increase in the expression of epithelial marker E⁃cadherin, and a decrease in the expression of mesenchymal markers Snail and Vimentin, were observed in Cx32⁃OE Huh7 cell line. Conclusion: Cx32 is low expressed in HCC tissues and cells, while the proliferation, migration and invasion ability of Huh7 cells can be inhibited by over⁃expression of Cx32, of which the underlying mechanism may be related to the inhibition of EMT process.

Effects of polydatin on the proliferation,migration,and invasion of ovarian cancer

To investigate the effects of polydatin on the proliferation,migration,and invasion of ovarian cancer,the change of proliferative ability,migration ability,and invasive ability of human ovarian cancer cell OVCAR-3,A2780,and HO-8910 was detected by using polydatin and up-regulating PI3K.The anticancer activity and mechanism of polydatin in ovarian cancer were analyzed.Polydatin could effectively inhibit the proliferation,migration,and invasion of OVCAR-3,A2780,and HO-8910,and inhibit the expression of PI3K protein.After the expression level of PI3K protein was up-regulated,the inhibitory effect of polydatin on the proliferative ability,migration ability,and invasive ability of OVCAR-3,A2780,and HO-8910 significantly decreased,suggesting that PI3K was the target of polydatin.Therefore,we concluded that polydatin could inhibit the proliferation,migration,and invasion of ovarian cancer cells by inhibiting the expression of PI3K protein,which provides an experimental basis for polydatin in the treatment of ovarian cancer.

TRIP13 is identified as a prognosis biomarker for renal clear cell carcinoma and promotes renal cell carcinoma cell proliferation, migration and invasion

This work aimed to discover new therapeutic targets in renal clear cell carcinoma by bioinformatics and detect the effect of candidate gene TRIP13 in renal cell carcinoma(RCC)cell proliferation,migration,and invasion.Differentially expressed mRNAs were screened based on The Cancer Genome Atlas(TCGA)-Kidney Renal Clear Cell Carcinoma(KIRC)databases,and functional enrichments,survival analysis,receiver operating characteristic curve(ROC),and Protein–Protein Interaction(PPI)protein interaction analysis were performed by R software to screen the candidate gene TRIP13.Then,the expression of candidate gene TRIP13 in 92 pairs of cancer and adjacent normal tissues of renal clear cell carcinoma patients were detected by qRT-PCR,western blotting,and immunochemical analysis.The TRIP13 level and clinicopathological characteristics of patients with renal clear cell carcinoma were analyzed.Using 186-O and ACHN RCC cell lines with TRIP13 overexpressing or downregulating,the effect of TRIP13 on cell viability and proliferation were detected by CCK8 and EdU staining,respectively.The migration and invasion were detected by Transwell assays.A total of 19858 differentially expressed genes,5823 differentially expressed genes,3657 up-regulated genes,and 2166 down-regulated genes were identified.TRIP13 was closed associated with cell cycle regulation,and survival and prognosis of renal clear cell carcinoma were selected as a candidate gene.The mRNA and protein levels of TRIP13 in cancer tissues were higher than that in adjacent normal tissues.TRIP13 level was significantly associated with tumor size,tumor stage,Fuhrman grade,and lymph node metastasis.TRIP13 overexpression significantly increased cell viability,proliferation,migration,and invasion,while downregulating of TRIP13 had opposite effects in both 186-O and ACHN cells.Therefore,TRIP13 promotes RCC proliferation and metastasis,which should be a novel biomarker for early diagnosis,treatment,and prognosis of RCC.

KIFC3 promotes proliferation, migration and invasion of esophageal squamous cell carcinoma cells by activating EMT and β-catenin signaling

BACKGROUND Esophageal squamous cell carcinoma(ESCC)is one of the most common malignancies.A total of 45 kinesin superfamily proteins(KIFs)have been identified in humans,among which several family members have demonstrated varied functions in tumor pathobiology via different mechanisms,including regulation of cell cycle progression and metastasis.KIFC3 has microtubule motor activity and is involved in cancer cell invasion and migration,as well as survival.However,the role of KIFC3 in ESCC is still unknown.AIM To evaluate the role of KIFC3 in ESCC and the underlying mechanisms.METHODS Expression of KIFC3 was evaluated in ESCC tissues and adjacent normal esophageal tissues.The prognostic value of KIFC3 was analyzed using Kaplan-Meier Plotter.Colony formation,EdU assays,cell cycle analysis,Transwell assay,immunofluorescence,and western blotting were performed in ESCC cell lines after transfection with pLVX-Puro-KIFC3-shRNA-and pLVX-Puro-KIFC3-expressing lentiviruses.A xenograft tumor model in nude mice was used to evaluate the role of KIFC3 in tumorigenesis.Inhibitor ofβ-catenin,XAV-939,was used to clarify the mechanism of KIFC3 in ESCC.To analyze the differences between groups,t test and nonparametric tests were used.P<0.05 was considered statistically significant.RESULTS Immunohistochemical staining indicated that KIFC3 was upregulated in ESCC tissues compared with adjacent normal tissues.Kaplan-Meier Plotter revealed that overexpressed KIFC3 was associated with poor prognosis in ESCC patients.Colony formation and EdU assay showed that KIFC3 overexpression promoted cell proliferation,while KIFC3 knockdown inhibited cell proliferation in ESCC cell lines.In addition,cell cycle analysis showed that KIFC3 overexpression promoted cell cycle progression.KIFC3 knockdown suppressed ESCC tumorigenesis in vivo.Transwell assay and western blotting revealed that KIFC3 overexpression promoted cell migration and invasion,as well as epithelial-mesenchymal transition(EMT),while KIFC3 knockdown showed the opposite results.Mechanistically,KIFC3 overexpression promoted β-catenin signaling in KYSE450 cells;however,the role of KIFC3 was abolished by XAV-939,the inhibitor of β-catenin signaling.CONCLUSION KIFC3 was overexpressed in ESCC and was associated with poor prognosis.Furthermore,KIFC3 promoted proliferation,migration and invasion of ESCC via β-catenin signaling and EMT.

miRNA-195:The New Target of Inhibiting the Proliferation,Migration and Invasion of Gastric Cancer Cells via Propofol

Objective:To explore the effect of propofol(Prof)on the proliferation,migration and invasion of human gastric cancer cell MGC-803 and its molecular mechanism.Methods:The MTT method was used to study the effects of Prof with different doses and durations on the viability of MGC-803 cells.Hoechst 33258 staining and electron microscopy were used to detect the effects of Prof on MGC-803 cell apoptosis.Transwell experiments were used to detect the effects of Prof on the migration and invasion of MGC-803 cells.RT-PCR detects the effect of Prof on the expression of miR-195 in MGC-803 cells,and Western Blot detects the effect of Prof on the protein expression of JAK/STAT signaling pathway.Results:Compared with 0μg/ml Prof,5μg/ml,10μg/ml and 20μg/ml Prof treatment with 24h,48h and 72h can significantly reduce cell viability(P<0.05).Compared with the Control group,the percentage of Hoechst 33258 staining positive cells in the Prof group and the apoptosis rate under the electron microscope were significantly increased(P<0.05).Compared with the Control group,the cell migration rate and invasion rate of the Prof group were significantly reduced(P<0.05).Compared with the Control group,the expression of miRNA-195 in the Prof group cells was increased significantly(P<0.05).Compared with the Control group,the activity of p-Jak1 and p-STAT3 proteins in the Prof group were significantly reduced(P<0.05).Conclusion:Prof can reduce the cell viability,migration and invasion of gastric cancer cell MGC-803,and promote its apoptosis.Its mechanism may be related to the promotion of miR-195 expression and inhibition of JAK/STAT signal pathway activity.

TM9SF1 is implicated in promoting the proliferation and invasion of bladder cancer cells

Zhuo et al looked into the part of transmembrane 9 superfamily member 1(TM9SF1)in bladder cancer(BC),and evaluated if it can be used as a therapeutic target.They created a permanent BC cell line and tested the effects of TM9SF1 overexpression and suppression on BC cell growth,movement,invasion,and cell cycle advancement.Their results show that TM9SF1 can boost the growth,movement,and invasion of BC cells and their access into the G2/M stage of the cell cycle.This research gives a novel direction and concept for targeted therapy of BC.

Effect of Interferon Regulatory Factor 1 on Proliferation,Invasion and Migration of Tongue Squamous Carcinoma Cells and Its Mechanism

[Objectives]This study was conducted to investigate the effect of interferon regulatory factor on the invasion and migration of tongue squamous carcinoma cells. [Methods]The expression level of IRF1 in tongue squamous carcinoma tissues was detected by real-time quantitative PCR and immunohistochemistry. Plasmids for overexpression and knockdown of IRF1 were constructed. The effects of overexpression and knockdown of IRF1 on the proliferation, invasion and migration of Tca8113 cells were examined in Tca8113 cells. [Results] IRF1 expression was abnormally reduced in tongue squamous carcinoma tissues, and both real-time quantitative PCR and immunohistochemistry showed significantly lower expression than that of paraneoplastic controls. The overexpression and knockdown plasmids of IRF1 were successfully constructed. Growth curve assays showed that overexpression of IRF1 inhibited the proliferation of Tca8113 cells, while knockdown of IRF1 promoted the proliferation of Tca8113 cells. Scratch assay showed that overexpression of IRF1 inhibited the migration of Tca8113 cells, while knockdown of IRF1 promoted the migration of Tca8113 cells. Transwell assay showed that overexpression of IRF1 inhibited the invasion of Tca8113 cells, while knockdown of IRF1 promoted the invasion of Tca8113 cells. [Conclusions] In the development of tongue squamous carcinoma, IRF1 functions as an anti-oncogene, and the expression level of IRF1 was reduced in tongue squamous carcinoma tissues.

High Expression of CDCA7 Promotes Cell Proliferation, Migration, Invasion and Apoptosis in Non-Small-Cell Lung Cancer

Objective Increased expression of CDCA7 is associated with a poorer prognosis in patients with non-small-cell lung cancer(NSCLC).This study was performed to investigate the effects of down-regulating cell division cycle-associated 7(CDCA7)gene expression on the proliferation,migration,invasion,cell cycle and apoptosis of human NSCLC cell lines.Methods Cultured A549 and NCI-H292 cells were transfected with si NC(control group)or si CDCA7(experimental group).Cell activity was detected using the CCK-8 and a Real Time Cell Analyzer(RTCA).Cell migration and invasion were also measured by RTCA.In addition,flow cytometry was used to assess the cell cycle progression and apoptosis in the cells,and Western blotting was used to detect the expression level of proteins in key signaling pathways.Results Compared with the cells transfected with si NC,the cell proliferation was significantly reduced(P<0.05),the migration and invasion were decreased,and the cell cycle was blocked in the G0/G1 phase(P<0.05)in the cells transfected with si CDCA7.The number of cells undergoing apoptosis was also increased(P<0.05).Western blotting revealed that P-ERK,Cyclin-D1,Vimentin and Bcl-2 were all downregulated.However,the expression of E-cadherin was not affected by the down-regulation of CDCA7,suggesting that it is upstream of this gene.Conclusion Silencing the CDCA7 gene inhibited the proliferation,migration and invasion of A549 and NCI-H292 cells,hindered the cell cycle transition to the S phase,and promoted cell apoptosis.These findings indicate that CDCA7 may represent a new therapeutic target for NSCLC.

Focal adhesion kinase signaling is necessary for the hydrogen sulfide-enhanced proliferation,migration,and invasion of HTR8/SVneo human trophoblasts

Objective:Hydrogen sulfide(H_(2)S)has been elucidated that it promotes migration and invasion in human placenta trophoblasts.However,the signaling pathway underlying H_(2)S-based regulation of trophoblasts remains unknown.Hence,we investigated the potential effect of sodium hydrosulfide(NaHS),an exogenous H_(2)S donor,on extravillous trophoblasts.Methods:The Cell Counting Kit-8 was used to detect the proliferative activity of trophoblasts and to screen the optimal concentration of NaHS.The migration and invasion of HTR8/SVneo cells were measured by Transwell assays.Gene expression was determined by quantitative real-time PCR analysis.Protein expression was determined by western blot.Results:We found that NaHS could promote the proliferation,migration,and invasion of HTR8/SVneo cells.The phosphorylation of focal adhesion kinase(FAK),Src,and extracellular signal-regulated kinase(ERK)were activated by NaHS.Moreover,NaHS also upregulated the expression of matrix metalloproteinase-2(MMP-2)and MMP-9,downregulated the expression of E-cadherin in HTR8/SVneo cells.The application of NaHS could increase the expression of cystathionine-β-synthase.Conclusion:Both FAK-Src signaling and the upstream signaling cascade of ERK activation play a significant important role in NaHS-induced proliferation,migration,and invasion via upregulating activity of MMP-2,MMP-9,and downregulating E-cadherin in HTR8/SVneo cells.These novel findings may provide a strong foundation for the clinical application of H_(2)S donor drugs.

Downregulation of miR-503 Promotes ESCC Cell Proliferation,Migration,and Invasion by Targeting Cyclin D1

Esophageal squamous cell carcinoma （ESCC） is one of the most aggressive cancers in China, but the underlying molecular mechanism of ESCC is still unclear. Involvement of micro- RNAs has been demonstrated in cancer initiation and progression. Despite the reported function of miR-503 in several human cancers, its detailed anti-oncogenic role and clinical significance in ESCC remain undefined. In this study, we examined miR-503 expression by qPCR and found the downregulation of miR-503 expression in ESCC tissue relative to adjacent normal tissues. Fur- ther investigation in the effect of miR-503 on ESCC cell proliferation, migration, and invasion showed that enhanced expression of miR-503 inhibited ESCC aggressive phenotype and overexpres- sion of CCND1 reversed the effect of miR-503-mediated ESCC cell aggressive phenotype. Our study further identified CCND1 as the target gene of miR-503. Thus, miR-503 functions as a tumor suppressor and has an important role in ESCC by targeting CCND1.

Anti-tumor activity of rice bran hydrolysates on migration, invasion and angiogenesis

Objective:To investigate anti-tumor effect of rice bran hydrolysates(RBH)on proliferation,migration,invasion,and angiogenesis of cholangiocarcinoma(CCA)cells,and elucidate the underlying mechanisms.Methods:RBH was prepared from Tubtim Chumprae rice(Oryza sativa L.)by hydrothermolysis followed by protease digestion.Phenolic content in RBH was analyzed by high-performance liquid chromatography.Human CCA cells,KKU-156,KKU-452,and KKU-100,were used to study the effects of RBH on proliferation,migration,invasion,and adhesion by wound healing,Transwell chamber,and fibronectin cell adhesion assays.Angiogenesis was evaluated using human umbilical vein endothelial cells.Proteins associated with cancer progression were analyzed by immunobloting assays.Results:RBH contained carbohydrates,proteins,lipids,and various phenolic compounds and flavonoids.RBH did not inhibit CCA proliferation,but strongly suppressed migration,invasion,adhesion of CCA cells,and the formation of tube-like capillary structures of human umbilical vein endothelial cells.Moreover,RBH downregulated phosphorylation of FAK,PI3K,and Akt,suppressed NF-κB nuclear translocation,decreased the expression of ICAM-1,vimentin and vascular endothelium growth factor(VEGF),and increased the expression of E-cadherin.Conclusions:RBH suppresses CCA cell migration and invasion and decreases expression of proteins involved in cancer metastasis.RBH is a potential food supplement for cancer prevention.

Knockdown of the Meq gene in Marek’s disease tumor cell line MSB1 might induce cell apoptosis and inhibit cell proliferation and invasion

Marek’s disease(MD),a highly cell-associated and contagious disease of chickens caused by Marek’s disease virus(MDV)can result in neural lesions,immunosuppression and neoplasia in chicken.The Meq gene is an important oncogene in the MDV genome,and it is expressed highly in MD tumor tissues and MD T-lymphoblastoid cell lines.An experiment was conducted to elucidate the role of Meq in MD tumor transformation.RNA interference technology was used to block its expression,and then analyzed the biological effects of Meq knockdown on the MD tumor cell line MSB1.A small interfering RNA with an interference efficiency of 70%(P<0.01)was transfected into MSB1 cells to knock down the expression of Meq gene.The cell proliferation,cycle and apoptosis were detected post-Meq knockdown.The results showed that MSB1 cell proliferation was downregulated remarkably at 48 h(P<0.01),60 h(P<0.05)and 72 h(P<0.01)post-Meq knockdown.The cell cycle was unaffected(P>0.05).B-cell lymphoma 2 gene(BCL2)was anti-apoptotic and caspase-6 was the effector in the apoptosis pathway.The activity of caspase-6 was upregulated(P<0.05)significantly and BCL2 gene expression was downregulated(P<0.05)significantly post-Meq knockdown,suggesting cell apoptosis might be induced.MSB1 cell migration did not exhibit any obvious change(P>0.05)post-Meq knockdown,but the expression of two genes(matrix metalloproteinase 2(MMP2)and MMP9)that are correlated closely to cell invasion was downregulated(P<0.05)remarkably post-Meq knockdown.The Meq knockdown might affect the main features of tumorous cells,including proliferation,apoptosis,and invasion,suggesting that the Meq gene might play a crucial role in interfering with lymphomatous cell transformation.

Tetrandrine suppresses proliferation, induces apoptosis, and inhibits migration and invasion in human prostate cancer cells

Tetrandrine （TET）, a traditional Chinese medicine, exerts remarkable anticancer activity on various cancer cells. However, little is known about the effect of TET on human prostate cancer cells, and the mechanism of function of TET on prostate cancer has not yet been elucidated. To investigate the effects of TET on the suppression of proliferation, induction of apoptosis, and inhibition of migration and invasion in human prostate cancer cell lines, DU145 and PC-3. Inhibition of growth was determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay and clone formation assay, and flow cytometry analysis was performed to detect the induction of apoptosis. Activation of poly （ADP-ribose） polymerase, caspase-3, Akt, phospho-Akt, Bcl-2, and Bax was analyzed by Western blotting. Wound healing assay and transwell migration assay were used to evaluate the effect of TET on migration and invasion of cancer cells. TET inhibited the growth of DU145 and PC-3 cells in a dose- and time-dependent manner. Cell cloning was inhibited in the presence of TET in DU145 and PC-3 cells. TET suppressed the migration of DU145 and PC-3 cells. Transwell invasion assay showed that TET significantly weakened invasion capacity of DU 145 and PC-3 cells. TET exhibited strong inhibitory effect on proliferation, migration, and invasion of prostate cancer cells. In addition, TET induced apoptosis in a dose-dependent manner by activating the caspase cascade and inhibiting phosphoinositide 3-kinase-Akt signal pathway. The accumulating evidence suggests that TET could be a potential therapeutic candidate against prostate cancer in a clinical setting.

Connective tissue growth factor as an unfavorable prognostic marker promotes the proliferation, migration, and invasion of gliomas

Background:In consideration of the difficulty in diagnosing high heterogeneous glioma,valuable prognostic markers are urgent to be investigated.This study aimed to verify that connective tissue growth factor(CTGF)is associated with the clinical prognosis of glioma,also to analyze the effect of CTGF on the biological function.Methods:In this study,glioma and non-tumor tissue samples were obtained in 2012 to 2014 from the Department of Neurosurgery of Nanfang Hospital of Southern Medical University,Guangzhou,China.Based on messenger RNA(mRNA)data from the Cancer Genome Atlas(TCGA)and CCGA dataset,combined with related clinical information,we detected the expression of CTGF mRNA in glioma and assessed its effect on the prognosis of glioma patients.High expression of CTGF mRNA and protein in glioma were verified by reverse transcription-polymerase chain reaction,immunohistochemistry,and Western blotting.The role of CTGF in the proliferation,migration,and invasion of gliomas were respectively identified by methylthiazoletetrazolium assay,Transwell and Boyden assay in vitro.The effect on glioma cell circle was assessed by flow cytometry.For higher expression of CTGF in glioblastoma(GBM),the biological function of CTGF in GBM was investigated by gene ontology(GO)analysis.Results:In depth analysis of TCGA data revealed that CTGF mRNA was highly expressed in glioma(GBM,n=163;lowly proliferative glioma[LGG],w=518;non-tumor brain tissue,n=207;LGG,t=2.410,GBM,t=2.364,P<0.05).CTGF mRNA and protein expression in glioma(86%)was significantly higher than that in non-tumor tissues(18%)verified by collected samples.Glioma patients with higher expression of CTGF showed an obviously poorer overall survival(35.4 and 27.0 months compared to 63.3 and 55.1 months in TCGA and Chinese Glioma Genome Atlas(CGGA)databases separately,CGGA:x2=7.596,P=0.0059;TCGA:x2=10.46,P=0.0012).Inhibiting CTGF expression could significantly suppress the proliferation,migration,and invasion of gliomas.CTGF higher expression had been observed in GBM,and GO analysis demonstrated that the function of CTGF in GBM was mainly associated with metabolism and energy pathways(P<0.001).Conclusions:CTGF is highly expressed in glioma,especially GBM,as an unfavorable and independent prognostic marker for glioma patients and fa&litates the progress of glioma.

Curcumin inhibits cervical cancer cell proliferation, migration and invasion by suppressing the PI3K/AKT signaling pathway via the miR-29b/KDM2A axis

In this study, we aimed to examine whether curcumin exerted its anti-tumor effects by regulating miR-29 b/KDM2 A in cervical cancer cells. The cell viability, migration and invasion were estimated in HeLa cervical cancer cells treated with curcumin. The effects of microRNA-29 b(miR-29 b) on biological behaviors of HeLa SiHa cells were also assessed. Potential target genes of miR-29 b were predicted and confirmed using a luciferase reporter assay, and the effects of curcumin and miR-29 b on the PI3 K/AKT signaling pathway were analyzed. Curcumin treatment inhibited cell proliferation, migration and invasion of HeLa cells(P<0.05). The miR-29 b expression was promoted by curcumin treatment in HeLa cells(P<0.01), and miR-29 b depletion could restore the effects of curcumin on cell proliferation, migration and invasion of HeLa cells(P<0.05). KDM2 A was proved as a direct target gene of miR-29 b, and the activity of the PI3 K/AKT signaling could be regulated by curcumin and miR-29 b(P<0.05). All the data revealed that curcumin played a protective role in cervical cancer. The proliferation, migration and invasion of cervical cancer cells were inhibited by curcumin through the miR-29 b/KDM2 A/PI3 K/AKT pathway.

Phosphoglycerate mutase 1 prostate cancer cell growth, knockdown inhibits migration, and invasion

Phosphoglycerate mutase 1 （PGAM1） is upregulated in many cancer types and involved in cell proliferation, migration, invasion, and apoptosis. However, the relationship between PGAM 1 and prostate cancer is poorly understood. The present study investigated the changes in PGAM1 expression in prostate cancer tissues compared with normal prostate tissues and examined the cellular function of PGAM1 and its relationship with clinicopathological variables. Immunohistochemistry and Western blotting revealed that PGAM 1 expression was upregulated in prostate cancer tissues and cell lines. PGAM 1 expression was associated with Gleason score （P = 0.01） and T-stage （P = 0.009）. Knockdown of PGAM 1 by siRNA in PC-3 and 22Rv I prostate cancer cell lines inhibited cell proliferation, migration, and invasion and enhanced cancer cell apoptosis. In a nude mouse xenograft model, PGAM1 knockdown markedly suppressed tumor growth. Deletion of PGAM1 resulted in decreased expression of Bcl-2, enhanced expression of Bax, caspases-3 and inhibition of MMP-2 and MMP-9 expression. Our results indicate that PGAM1 may play an important role in prostate cancer progression and aggressiveness, and that it might be a valuable marker of poor prognosis and a potential therapeutic target for prostate cancer.

Effects of miR-200c on the migration and invasion abilities of human prostate cancer Du145 cells and the corresponding mechanism

microRNAs （miRNAs） have played a key role in human tumorigenesis, tumor progression, and metastasis. On the one hand, miRNAs are aberrantly expressed in many types of human cancer; on the other hand, miRNAs can function as tumor suppressors or oncogenes that target many cancer-related genes. This study aimed to investigate the effects of miRNA-200c （miR-200c） on the biological behavior and mechanism of proliferation, migration, and invasion in the prostate cancer cell line Du145. In this study, Du145 cells were transfected with miR-200c mimics or negative control miR-NC by using an X-tremeGENE siRNA transfection reagent. The relative expression of miR-200c was measured by RT-PCR. The proliferation, migration, and invasion abilities of Du145 cells were detected by CCK8 assays, migration assays and invasion assays, respectively. The expressions of ZEB1, E-cadherin, and vimentin were observed by western blot. Results showed that DU145 cells exhibited a high expression of miR-200e compared with immortalized normal prostate epithelial cell RWPE-1. Du145 cells were then transfected with miR-200c mimics and displayed lower abilities of proliferation, migration, and invasion than those transfected with the negative control. The protein levels of ZEB1 and vimentin were expressed at a low extent in Du145 cells, which were transfected with miR-200c mimics; by contrast, E-cadherin was highly expressed. Hence, miR-200c could significantly inhibit the proliferation of the prostate cancer cell line Du145; likewise, miR- 200c could inhibit migration and invasion by epithelial-mesenchymal transition.

Nonlinear Evolution Equations and Its Application to a Tumour Invasion Model

We consider nonlinear evolution equations with logistic term satisfying initial Neumann-boundary condition and show global existence in time of solutions to the problem in arbitrary space dimension by using the method of energy. Applying the result to a mathematical model of tumour invasion, we discuss the property of the rigorous solution to the model. Finally we will show the time depending relationship and interaction between tumour cells, the surrounding tissue and matrix degradation enzymes in the model by computer simulations. It is seen that our mathematical result of the existence and asymptotic behaviour of solutions verifies our simulations, which also confirm the mathematical result visibly.

Has_circ_0000069 expression in breast cancer and its influences on prognosis and cellular activities

Circular RNA(circRNA),as a newly discovered non-coding RNA with important regulatory potential,is closely related to the occurrence and progression of various tumors.This study aimed to investigate has_circ_0000069 expression in breast cancer and its influence on cellular activities.Using real-time quantitative polymerase chain reaction,has_circ_0000069 levels were measured in 137 pairs of tissue specimens,as well as cancer cell lines.The cellular activities of cell lines were determined by cell counting kit-8(CCK-8)and Transwell assays.The potential targeting miRNAs were predicted and verified using an online database and dual-luciferase reporter assay.Has_circ_0000069 was highly expressed in breast cancer tissues and cells.The expression of has_circ_0000069 was associated with the five-year overall survival of patients.After silencing has_circ_0000069 in breast cancer cells,its expression reduced,and the ability of cell proliferation,migration,and invasion decreased.MiR-432 was verified as a targeting miRNA of has_circ_0000069.Has_circ_0000069 expression increased in breast cancer and was negatively related to patient’s prognosis.Has_circ_0000069 may facilitate breast cancer tumor progression by sponging miR-432.These findings revealed that has_circ_0000069 may be a biomarker for predicting prognosis and a therapeutic target for treating patients with breast cancer.