At present,the role of many long non-coding RNAs(lncRNAs)as tumor suppressors in the formation and development of cervical cancer(CC)has been studied.However,lncRNA prostate cancer gene expression marker 1(PCGEM1),who...At present,the role of many long non-coding RNAs(lncRNAs)as tumor suppressors in the formation and development of cervical cancer(CC)has been studied.However,lncRNA prostate cancer gene expression marker 1(PCGEM1),whose high expression not only aggravates ovarian cancer but also can induce tumorigenesis and endometrial cancer progression,has not been studied in CC.The objective of this study was to investigate the expression and the underlying role of PCGEM1 in CC.The relative expression of PCGEM1 in CC cells was detected by real-time PCR.After the suppression of PCGEM1 expression by shRNA,the changes in the proliferation,migration,and invasion capacities were detected via CCK-8 assay,EdU assay,and colony formation assay wound healing assay.Transwell assay and the changes in expressions of epithelial-to-mesenchymal transition(EMT)markers were determined by western blot and immunofluorescence.The interplay among PCGEM1,miR-642a-5p,and kinesin family member 5B(KIF5B)was confirmed by bioinformatics analyses and luciferase reporter assay.Results showed that PCGEM1 expressions were up-regulated within CC cells.Cell viabilities,migration,and invasion were remarkably reduced after the suppression of PCGEM1 expression by shRNA in Hela and SiHa cells.N-cadherin was silenced,but E-cadherin expression was elevated by sh-PCGEM1.Moreover,by sponging miR-642a-5p in CC,PCGEM1 was verified as a competitive endogenous RNA(ceRNA)that modulates KIF5B levels.MiR-642a-5p down-regulation partially rescued sh-PCGEM1’s inhibitory effects on cell proliferation,migration,invasion,and EMT process.In conclusion,the PCGEM1/miR-642a-5p/KIF5B signaling axis might be a novel therapeutic target in CC.This study provides a research basis and new direction for targeted therapy of CC.展开更多
癫痫持续状态(status epilepticus,SE)是儿童急重症,年均发病率17~23/10万[1],控制不佳易转变为难治性癫痫持续状态(refractory status epilepticus,RSE),其中通过全身麻醉治疗24h后发作仍未终止的RSE被称为超级难治性癫痫持续状态(supe...癫痫持续状态(status epilepticus,SE)是儿童急重症,年均发病率17~23/10万[1],控制不佳易转变为难治性癫痫持续状态(refractory status epilepticus,RSE),其中通过全身麻醉治疗24h后发作仍未终止的RSE被称为超级难治性癫痫持续状态(super refractory status epilepticus,SRSE),SRSE是一种罕见的破坏性疾病,儿童SRSE的病死率可达13.3%[2],若未经及时救治,可导致机体内环境紊乱、多脏器功能障碍等,甚至危及生命,存活者往往存在不同程度的脑损伤。展开更多
Objective: To investigate the mechanism of cell cyclin-dependent kinase (KDM5B), a key enzyme driving all cell cycle transitions, promoting HCC progression and metastasis. Methods: The expression of KDM5B in normal li...Objective: To investigate the mechanism of cell cyclin-dependent kinase (KDM5B), a key enzyme driving all cell cycle transitions, promoting HCC progression and metastasis. Methods: The expression of KDM5B in normal liver, HCC and its adjacent tissues was analyzed by RT-PCR and IHC. Lentivirus transfection method was used to construct stable cell lines with KDM5B overexpression and down-regulation, and the role of KDM5B in HCC migration and invasion was detected at cell level and animal level. Western blotting and Transwell experiments were performed to verify the effect of KDM5B and/or CCR2 inhibitors on HCC progression and metastasis by using liver orthotopic transplantation tumor model and immunofluorescence methods. Results: RT-PCR showed that the expression level of KDM5B in HCC was significantly higher than that in adjacent tissues, and the increase of KDM5B was relatively significant. Upregulation of KDM5B in nude mouse liver orthotopic transplantation tumor model can promote the incidence of lung metastasis and shorten the survival time of nude mice, whereas upregulation of KDM5B can reduce the incidence of lung metastasis and prolong the survival time of nude mice. Conclusion: This study clarified the expression of KDM5B in HCC and its function in promoting HCC migration, invasion and metastasis. The molecular mechanism of KDM5B promoting HCC metastasis was revealed, providing a potential therapeutic target for HCC.展开更多
基金the Nantong Municipal Health Commission Research Project(MB2021054)for this study.
文摘At present,the role of many long non-coding RNAs(lncRNAs)as tumor suppressors in the formation and development of cervical cancer(CC)has been studied.However,lncRNA prostate cancer gene expression marker 1(PCGEM1),whose high expression not only aggravates ovarian cancer but also can induce tumorigenesis and endometrial cancer progression,has not been studied in CC.The objective of this study was to investigate the expression and the underlying role of PCGEM1 in CC.The relative expression of PCGEM1 in CC cells was detected by real-time PCR.After the suppression of PCGEM1 expression by shRNA,the changes in the proliferation,migration,and invasion capacities were detected via CCK-8 assay,EdU assay,and colony formation assay wound healing assay.Transwell assay and the changes in expressions of epithelial-to-mesenchymal transition(EMT)markers were determined by western blot and immunofluorescence.The interplay among PCGEM1,miR-642a-5p,and kinesin family member 5B(KIF5B)was confirmed by bioinformatics analyses and luciferase reporter assay.Results showed that PCGEM1 expressions were up-regulated within CC cells.Cell viabilities,migration,and invasion were remarkably reduced after the suppression of PCGEM1 expression by shRNA in Hela and SiHa cells.N-cadherin was silenced,but E-cadherin expression was elevated by sh-PCGEM1.Moreover,by sponging miR-642a-5p in CC,PCGEM1 was verified as a competitive endogenous RNA(ceRNA)that modulates KIF5B levels.MiR-642a-5p down-regulation partially rescued sh-PCGEM1’s inhibitory effects on cell proliferation,migration,invasion,and EMT process.In conclusion,the PCGEM1/miR-642a-5p/KIF5B signaling axis might be a novel therapeutic target in CC.This study provides a research basis and new direction for targeted therapy of CC.
文摘癫痫持续状态(status epilepticus,SE)是儿童急重症,年均发病率17~23/10万[1],控制不佳易转变为难治性癫痫持续状态(refractory status epilepticus,RSE),其中通过全身麻醉治疗24h后发作仍未终止的RSE被称为超级难治性癫痫持续状态(super refractory status epilepticus,SRSE),SRSE是一种罕见的破坏性疾病,儿童SRSE的病死率可达13.3%[2],若未经及时救治,可导致机体内环境紊乱、多脏器功能障碍等,甚至危及生命,存活者往往存在不同程度的脑损伤。
文摘Objective: To investigate the mechanism of cell cyclin-dependent kinase (KDM5B), a key enzyme driving all cell cycle transitions, promoting HCC progression and metastasis. Methods: The expression of KDM5B in normal liver, HCC and its adjacent tissues was analyzed by RT-PCR and IHC. Lentivirus transfection method was used to construct stable cell lines with KDM5B overexpression and down-regulation, and the role of KDM5B in HCC migration and invasion was detected at cell level and animal level. Western blotting and Transwell experiments were performed to verify the effect of KDM5B and/or CCR2 inhibitors on HCC progression and metastasis by using liver orthotopic transplantation tumor model and immunofluorescence methods. Results: RT-PCR showed that the expression level of KDM5B in HCC was significantly higher than that in adjacent tissues, and the increase of KDM5B was relatively significant. Upregulation of KDM5B in nude mouse liver orthotopic transplantation tumor model can promote the incidence of lung metastasis and shorten the survival time of nude mice, whereas upregulation of KDM5B can reduce the incidence of lung metastasis and prolong the survival time of nude mice. Conclusion: This study clarified the expression of KDM5B in HCC and its function in promoting HCC migration, invasion and metastasis. The molecular mechanism of KDM5B promoting HCC metastasis was revealed, providing a potential therapeutic target for HCC.
