Deleted in liver cancer 1 suppresses the growth of prostate cancer cells through inhibiting Rho-associated protein kinase pathway

Objective:Deleted in liver cancer 1(DLC1)is a GTPase-activating protein that is reported as a suppressor in certain human cancers.However,the detailed biological function of DLC1 is still unclear in human prostate cancer(PCa).In the present study,we aimed to explore the function of DLC1 in PCa cells.Methods:Silencing and overexpression of DLC1 were induced in an androgen-sensitive PCa cell line(LNCaP)using RNA interference and lentiviral vector transduction.The Cell Counting Kit-8 assay was performed to determine cell proliferation.The cell cycle was examined by performing a propidium iodide staining assay.Results:Our results indicated that DLC1 overexpression markedly suppressed the proliferation and cell cycle progression of LNCaP cells.Moreover,DLC1 expression was negatively correlated with Rho-associated protein kinase(ROCK)expression in LNCaP cells.Importantly,this study showed that the ROCK inhibitor Y27632 restored the function of DLC1 in LNCaP cells and reduced the tumorigenicity of LNCaP cells in vivo.Conclusion:Our results indicated that DLC1 overexpression markedly suppressed the proliferation and cell cycle progression of PCa cells and negatively correlated with ROCK expression in PCa cells and tissue.

Nerve growth factor pretreatment against glutamate-induced hippocampal neuronal injury Action mechanism of phosphatase and tensin homologue deleted on chromosome 10

BACKGROUND： Nerve growth factor （NGF） attenuates glutamate-induced injury to hippocampal neurons, and the human tumor suppressor gene phosphatase and tensin homologue deleted on chromosome 10 （PTEN） promotes neuronal apoptosis. However, effects of PTEN in NGF-mediated neuroprotection against glutamate excitotoxicity remain poorly understood. OBJECTIVE： To investigate the relationship between NGF inhibition of glutamate-induced injury and PTEN. DESIGN, TIME AND SE＇I＇rlNG： The randomized, controlled, in vitro study was performed at the Department of Pathophysiology, Medical School of Nantong University, China from October 2007 to March 2008. MATERIALS： Glutamate, NGF, 4, 6-diamidino-2-phenyl-indolediacetate, 3-[4, 5-dimethylthiazol-2-yl]- 2, 5-diphenyl tetrazoliumbromide （M-I-F）, and lactate dehydrogenase kit （Sigma, USA）, fluorescence microscope and inverted phase contrast microscope （Olympus, Japan） were used in this study. METHODS： Hippocampal neurons were obtained from newborn （〈 24 hours） Sprague Dawley rats and cultured for 7 days. The control group was not treated with any intervention factor, the glutamate group was treated with glutamate （0.2 mmol/L）, and NGF groups were treated with NGF （10, 50, 100, and 200 μg/L, respectively） prior to glutamate treatment. MAIN OUTCOME MEASURES： The MTT and lactate dehydrogenase assays were applied to evaluate viability of hippocampal neurons. Morphological changes in hippocampal neurons were observed using an inverted phase-contrast microscope, and neuronal apoptosis was detected by 4, 6-diamidino-2- phenyl-indolediacetate staining. PTEN mRNA and protein expression were measured by reverse transcription-polymerase chain reaction and Western blot analysis, respectively. RESULTS： Glutamate （0.2 mmol/L） induced significantly decreased neuronal viability and greater lactate dehydrogenase efflux compared with the control group （P 〈 0.01）. However, compared with the glutamate group, cell viability significantly increased and lactate dehydrogenase efflux decreased in the NGF group with increasing NGF concentrations （P 〈 0.05 or P 〈 0.01）. The apoptotic ratio and PTEN mRNA and protein expression decreased in the NGF group compared with the glutamate group （P 〈 0.01）. CONCLUSION： Pretreatment with NGF exerted neuroprotective effects against glutamate-induced injury, partially through inhibition of PTEN expression and neuronal apoptosis.

Effects and mechanism of adenovirus-mediated phosphatase and tension homologue deleted on chromosome ten gene on collagen deposition in rat liver fibrosis

AIM To evaluate the effects of phosphatase and tension homologue deleted on chromosome ten(PTEN) gene on collagen metabolism in hepatic fibrosis and the underlying mechanisms.METHODS rat primary hepatic stellate cells(HSCs) and human LX-2 cells were transfected with adenovirus containing c DNA constructs encoding wild-type PTEN(Ad-PTEN), PTEN mutant G129 E gene(Ad-G129E), and r NA interference constructs targeting the PTEN sequence PTEN short hairpin r NA to up-regulate and downregulate the expression of PTEN. HSCs were assayed using fluorescent microscopy, real-time polymerase chain reaction, and western blotting. Moreover, a CCl_4-induced rat hepatic fibrosis model was established to investigate the in vivo effects. Hematoxylin and eosin, and Masson's trichrome were used to assess the histological changes. The expression of collagen Ⅰ and Ⅲ was assessed using immunohistochemistry and western blot analysis.RESULTS Elevated expression of PTEN gene reduced serum levels of alanine transaminase and aspartate transaminase, decreased collagen deposition in the liver, and reduced hepatocyte necrosis. In contrast, knockdown of PTEN expression had an opposite effect, such as increased collagen deposition in the liver, and was molecularly characterized by the increased expression of matrix metalloproteinase(MMP)-13(P < 0.01) and MMP-2(P < 0.01), as well as decreased expression of the tissue inhibitor of metalloproteinase(TIMP)-1(P < 0.01) and TIMP-2(P < 0.01).CONCLUSION These data indicated that gene therapy using recombinant adenovirus encoding PTEN might be a novel way of treating hepatic fibrosis.

Tumor suppressor genes on frequently deleted chromosome 3p in nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is among the most common malignancies in southern China.Deletion of genomic DNA,which occurs during the complex pathogenesis process for NPC,represents a pivotal mechanism in the inactivation of tumor suppressor genes (TSGs).In many circumstances,loss of TSGs can be detected as diagnostic and prognostic markers in cancer.The short arm of chromosome 3 (3p) is a frequently deleted chromosomal region in NPC,with 3p21.1-21.2 and 3p25.2-26.1 being the most frequently deleted minimal regions.In recent years,our research group and others have focused on the identification and characterization of novel target TSGs at 3p,such as RASSF1A,BLU,RBMS3,and CHL1,in the development and progression of NPC.In this review,we summarize recent findings of TSGs at 3p and discuss some of these genes in detail.A better understanding of TSGs at 3p will significantly improve our understanding of NPC pathogenesis,diagnosis,and treatment.

Expression of netrin-1 and its receptors, deleted in colorectal cancer and uncoordinated locomotion-5 homolog B, in rat brain following focal cerebral ischemia reperfusion injury

Netrin-1 is currently one of the most highly studied axon guidance factors. Netrin-1 is widely expressed in the embryonic central nervous system, and together with the deleted in colorectal cancer and uncoordinated locomotion-5 homolog B receptors, netrin-1 plays a guiding role in the construction of neural conduction pathways and the directional migration of neuronal cells. In this study, we established a rat middle cerebral artery ischemia reperfusion model using the intraluminal thread technique. Immunofluorescence microscopy showed that the expression of netrin-1 and deleted in colorectal cancer in the ischemic penumbra was upregulated at 1 day after reperfusion, reached a peak at 14 days, and decreased at 21 days. There was no obvious change in the expression of uncoordinated locomotion-5 homolog B during this time period. Double immunofluorescence labeling revealed that netrin-1 was expressed in neuronal cells and around small vessels, but not in astrocytes and microglia, while deleted in colorectal cancer was localized in the cell membranes and protrusions of neurons and astrocytes. Our experimental findings indicate that netrin-1 may be involved in post-ischemic repair and neuronal protection via deleted in colorectal cancer receptors.

Expression of Porcine Interleukin-2 and Porcine Interleukin-6 and Their Adjuvant Effects on Gene Deleted Vaccine of Pseudorabies Virus(TK^-/gG^-/LacZ^+)

Porcine interleukin-2 and porcine interleukin-6 cDNA sequences were cloned into the expressing vectors pET-28a and pGEX-KG respectively. They were expressed in E. coli BL21(DE3)with high-level production. The gene deleted vaccine of pseudorabies virus Ea strain(TK-/gG-/LacZ+)was mixed with the two different purified recombinant proteins each, or both, with the doses of 2, 5 or 10 μg ml-1. Ten groups of pseudorabies negative antibody swines were immuned twice with tested vaccines with different doses, or control vaccine, respectively. The antibody liters of the test groups were detected by neutralization test, and the daily weight gains of swines were calculated and analyzed statistically. In the study, all the neutralizing antibody ti-ters in test groups were higher than the control group, and the recombinant proteins appeared a dose dependent adjuvant effect. The tested vaccines with 2 μg ml-1 pIL-2 and with 10 μg ml-1 pIL-2/pIL-6 got significant and extremely significant differences, compared with the vaccines without pILs. The difference of the daily weight gain indicated the potential positive influence of pIL-2 and pIL-6 on immune protection.

Research Progress on Pseudorabies Gene-deleted Vaccine

Pseudorabies is caused by pseudorabies virus (PrV), which is a member of family Herpesviridae, subfamily Alphaherpesvirinae and is the agent of acute infectious disease in many domestic and wild animals. Swine was the natural host and reservior of PRV, which inflicts major economic loss in pig industries world wide. Immunization with safe, effective vaccine is main measurements to prevent the disease. In this assay, research progress on PRV gene-deleted vaccine used extensively today was discussed.

Influence of Deleted in Colorectal Carcinoma Gene on Proliferation of Ovarian Cancer Cell Line SKOV-3 In Vivo and In Vitro

Objective To elucidate the effects of the deleted in colorectal carcinoma(DCC) gene on proliferation of ovarian cancer cell line SKOV-3.Method An exogenous recombinant eukaryotic expression vector pcDNA3.1(+)-DCC,containing human DCC cDNA coding sequences,was constructed and transfected into SKOV-3 cells(SKOV-3/DCC).The pcDNA3.1(+) transfected cells(SKOV-3/Neo) and SKOV-3 cells were used as the positive and negative controls,respectively.Expressions of DCC mRNA and protein were analyzed by RT-PCR and immunocytochemical analysis,respectively.Cell growth was detected by soft agar colony formation assay and MTT assay.Flow cytometry and transmission electron microscopy were used to assess the effects of DCC on cell cycle distribution and ultrastructure,respectively.BALB/c mice were used to evaluate the effects of DCC on tumorigenicity in vivo.Results RT-PCR and immunocytochemical analysis revealed the exogenous DCC gene was successfully transfected into SKOV-3 cell lines and obtained permanent expression.The half maximal inhibitory concentration(IC50) of SKOV-3/DCC cells was significantly lower than that of SKOV-3 or SKOV-3/Neo cells(all P<0.05).DCC expression caused SKOV-3 cells to be arrested in G1 phase(78.0%),and electron microscopic analysis showed SKOV-3/DCC cells displayed typical morphological changes of apoptosis.Two mice xenografted with SKOV-3/DCC cells showed no tumor tumorigenecity.The tumor volume of BALB/c mice bearing SKOV-3/DCC cells(3.403 mm3) was smaller than that of SKOV-3 cells(9.206 mm3).Conclusion DCC gene may play an important role in suppressing the growth of SKOV-3 cell line and inducing apoptosis.

Novel Deletion in Exon 7 of Betaine Aldehyde Dehydrogenase 2(BADH2)

The fragrance of rice is one of the premium characteristics that breeders want to include in rice varieties due to the higher market value. Nucleotide deletions in exons 2(7 bp) and 7(8 bp) of Betaine Aldehyde Dehydrogenase 2(BADH2) are associated with fragrance in rice. In this study, a new 13 bp deletion in exon 7 of the BADH2 gene was discovered in the Nang Thom Cho Dao(NTCD) variety, and the mutation has been closely related to the genetic background of indica subspecies through the Bayesian phylogenetic approach and haplotype network analysis of the 3 000 Rice Genomes Project. In addition, a set of functional markers(EX07-13F, EX07-13RN, and EX07-13RM) identified the 13 bp deletion only within NTCD(no amplified band) compared with both non-aromatic and other aromatic rice varieties(110 bp band). The deletion of 13 bases instead of 8 bases in exon 7 of BADH2 caused a premature stop codon, which down-regulated the expression of the BADH2 transcript while associated with up-regulation of OsP5CS and the high amount of 2-acetyl-1-pyrroline. It is potential to use the deletion in exon 7 of the BADH2 gene as a novel marker for adulteration and breeding of fragrant rice varieties, particularly for NTCD.

BD: business.deleted

“我Kao!”,胡一郎看到新的工作任务,差点没把嘴里的茶全喷了。“BD部门近期工作重点:与电信部门洽谈向手机用户提供奥运快讯短信息服务事宜。”胡一郎在脑子里飞快地计算:一条短信息中国移动才向用户收费一毛,公司最多能挣几分钱?My God!原来“最清晰的可盈利电子商务模式”就是挣这点没影儿的钱? 做了这几个月的BD,胡一郎觉得自己彻底晕菜。过去做销售,目的明确,实打实地挣钱;现在可好,找谁?说什么?谈得成谈不成?似乎都不重要,谈成的项目保不齐也会被公司cancel,真不知道自己的工作究竟有什么意义。

De novel heterozygous copy number deletion on 7q31.31-7q31.32 involving TSPAN12 gene with familial exudative vitreoretinopathy in a Chinese family

AIM:To investigate the genetic and clinical characteristics of patients with a large heterozygous copy number deletion on 7q31.31-7q31.32.METHODS:A family with familial exudative vitreoretinopathy(FEVR)phenotype was included in the study.Whole-exome sequencing(WES)was initially used to locate copy number variations(CNVs)on 7q31.31-31.32,but failed to detect the precise breakpoint.The long-read sequencing,Oxford Nanopore sequencing Technology(ONT)was used to get the accurate breakpoint which is verified by quantitative real-time polymerase chain reaction(QPCR)and Sanger Sequencing.RESULTS:The proband,along with her father and younger brother,were found to have a heterozygous 4.5 Mb CNV deletion located on 7q31.31-31.32,which included the FEVRrelated gene TSPAN12.The specific deletion was confirmed as del(7)(q31.31q31.32)chr7:g.119451239_123956818del.The proband exhibited a phase 2A FEVR phenotype,characterized by a falciform retinal fold,macular dragging,and peripheral neovascularization with leaking of fluorescence.These symptoms led to a significant decrease in visual acuity in both eyes.On the other hand,the affected father and younger brother showed a milder phenotype.CONCLUSION:The heterozygous CNV deletion located on 7q31.31-7q31.32 is associated with the FEVR phenotype.The use of long-read sequencing techniques is essential for accurate molecular diagnosis of genetic disorders.

Deletion and Recovery Scheme of Electronic Health Records Based onMedical Certificate Blockchain

The trusted sharing of Electronic Health Records(EHRs)can realize the efficient use of medical data resources.Generally speaking,EHRs are widely used in blockchain-based medical data platforms.EHRs are valuable private assets of patients,and the ownership belongs to patients.While recent research has shown that patients can freely and effectively delete the EHRs stored in hospitals,it does not address the challenge of record sharing when patients revisit doctors.In order to solve this problem,this paper proposes a deletion and recovery scheme of EHRs based on Medical Certificate Blockchain.This paper uses cross-chain technology to connect the Medical Certificate Blockchain and the Hospital Blockchain to real-ize the recovery of deleted EHRs.At the same time,this paper uses the Medical Certificate Blockchain and the InterPlanetary File System(IPFS)to store Personal Health Records,which are generated by patients visiting different medical institutions.In addition,this paper also combines digital watermarking technology to ensure the authenticity of the restored electronic medical records.Under the combined effect of blockchain technology and digital watermarking,our proposal will not be affected by any other rights throughout the process.System analysis and security analysis illustrate the completeness and feasibility of the scheme.

Rapid construction of phosphatase and tensin homolog-deleted on chromosome ten gene recombinant adenovirus using the AdEasy system

Recent studies have shown that phosphatase and tensin homolog-deleted on chromosome ten （PTEN） gene plays an important role in ischemic brain damage and synaptic plasticity. The AdEasy system, which has been widely used, greatly simplifies preparation of recombinant adenovirus. Therefore, recombinant defective adenovirus vector carrying human PTEN tumor suppressor gene （Ad-PTEN） was constructed using the AdEasy-1 system and was transfected into HEK293 cells for packaging and amplification. Infection efficiency and expression intensity were observed in primary cultured rat hippocampal neurons infected with Ad-PTEN in vitro. Results revealed a cytopathic effect in green fluorescent protein expression, which increased with prolonged time. After three cycles of amplification, the adenovirus titer was increased to an adequate titer for infecting hippocampal neurons. The entire process typically requires 4-5 weeks for completion. Results suggested that recombinant defective adenovirus vector carrying the PTEN gene was successfully and rapidly constructed using the AdEasy system.

Phosphatase and tensin homology deleted in chromosome 10,hypoxia-inducible factor-1 alpha gene expression in colorectal adenoma and adenocarcinoma and their relation to vascular endothelial growth factor protein expression

To examine phosphatase and tensin homology deleted in chromosome 10 (PTEN),hypoxia-inducible factor-1 alpha (HIF-1 alpha) gene expressions and their relation to vascular endothelial growth factor(VEGF) protein expression in the patients with human colorectal adenomas and adenocarcinomas.Methods The expression of PTEN,HIF-1 alpha gene was detected by using in situ hybridization,and the VEGF expression levels by immunohistochemistry in colorectal adenomas and primary colorectal adenocarcinoma.Results Strong expression of HIF-1 alpha was detectable in the majority of colorectal dadenocarcinoma,particularly surrounding areas of necrosis in adenocarcinoma.PTEN,HIF-1 alpha mRNA and VEGF protein were positive in 51.6%,67.7% and 59.7% respectively in 62 cases of adenocarcinomas,and 77.8%,44.4% and 33.3% respectively in 18 cases of adenomas.The positive rate of VEGF was higher in the patients with colorectal adenocarcinomas than that in those with adenomas,whereas that of PTEN mRNA was contrary.HIF-1 mRNA expression was correlated significantly with lymph node metastasis,liver metastasis,Duke’s stage and recurrence.During colorectal tumor progression,the expression of HIF-1 alpha mRNA was positively correlated with the VEGF protein expression (χ2= 4.751 ,P<0.05),but negatively with the PTEN mRNA expression(χ2=21.84,P<0.01).Conclusion The absence or low expression of PTEN and the increased levels of HIF-1α and VEGF may paly an important role in carcinogenesis and progression of colorectal carcinoma.These results suggest that VEGF upregulated by HIF-1 alpha gene may be involved in angiogenesis of colorectal adenocarcinoma.4 refs,1 tab.

基于重测序的23份香菇种质资源全基因组序列分析

为了对河南香菇主产区的主栽品种进行鉴定,并分析其遗传多样性,将河南主栽的23份香菇种质资源进行重测序,对单核苷酸多态性(single nucleotide polymorphism,SNP)和小片段插入缺失(insertion-deletion,InDel)等数据进行统计和分析,并基于SNP变异对23份香菇资源进行遗传结构分析、进化树构建和主成分分析。结果表明,在23份香菇样本中,比对到参考基因组上的reads数目占总数的比例范围为72.53%~90.60%,样品平均测序深度范围为12.83~19.99,覆盖率范围为91.89%~99.32%。SNP位点共计14115075个,InDel共计1909516个。23份香菇样本的群体遗传结构及系统发育分析表明其包含3个谱系,遗传距离0.05490~0.65689,推测它们至少有3个祖先遗传成分。结合主成分分析法明确各菌种间的亲缘关系远近,证明了菌种分支具有明显的地域性。综合分析表明,以基因序列相似度、遗传距离差异及亲缘关系远近为主要依据特点,有助于对香菇地方品种命名和其特征特性关系的认识,促进优异种质资源的交流与利用。

一例Xq22.3q27.3缺失患者的遗传学分析

目的:对1例无相关特异表型的Turner综合征患者进行遗传学分析,为临床医生识别女性X染色体偏倚失活提供参考。方法:采集1例原发不孕3年的女性及其丈夫和父母的外周静脉血,行染色体核型分析、女方染色体拷贝数变异(CNVs)检测,并进行遗传学分析。结果:原发不孕患者外周血染色体核型为46,X,del(X)(q22.3),其父母及丈夫染色体核型结果均正常。患者CNVs结果提示X染色体q22.3-q27.3缺失40.62Mb,为致病性改变。患者缺失的X染色体失活偏倚比例为98:2,为X染色体极度失活偏倚。结论:临床医生应考虑到女性患者存在X染色体偏倚失活的可能,尽早发现染色体异常患者,以避免生育风险及出生缺陷的发生。

基于EWM-AHP-RF的改进灰色关联云数据确定性删除效果评价

针对当前数据确定性删除效果受多因素影响、难以客观评价的问题,提出一种基于熵权法-层次分析法-随机森林(EWM-AHP-RF)确定权重的方法,并与改进的灰色关联模型相结合,对云数据确定性删除方案进行了删除效果的组合评价。首先,构建了删除效果评价指标体系;然后,将熵权法和层次分析法进行结合,确定了指标的组合权重,并基于随机森林方法进行权重的更新;最后,基于改进灰色关联评价模型对云数据确定性删除方案的删除效果进行了评价。结果验证了所提方法的有效性和科学性。

间充质干细胞外泌体对缺血性脑卒中大鼠神经功能恢复的影响

目的探讨间充质干细胞外泌体(MSCs-EXO)对缺血性脑卒中大鼠神经功能恢复的影响。方法大鼠骨髓间充质干细胞原代培养,超速离心法提取其MSCs-EXO,大脑中动脉夹闭模型(MCAO)法制作大鼠缺血性脑卒中模型,MSCs-EXO经鼻给药,设为MSCs-EXO组,通过改良神经功能缺损评分(mNSS)和错步试验评估其神经功能恢复情况,并与未治疗模型组(MCAO组)做对比。PKH26标记MSCs-EXO并结合免疫荧光染色观察其在缺血半暗带(IP)中的分布,荧光定量PCR及Western blot检测IP区域脑组织中PTEN的表达水平,并与正常大鼠及MCAO组大鼠进行对比。结果MSCs-EXO治疗组的神经功能恢复高于MCAO组,差异有统计学意义(P<0.05)。免疫荧光染色显示标记外泌体可以进入IP区域神经细胞,荧光定量PCR及Western blot检测显示MSCs-EXO治疗组及MCAO组中PTEN水平均较正常升高,但MSCs-EXO治疗组的PTEN水平低于MCAO组,差异有统计学意义(P<0.05)。结论MSCs-EXO能够促进缺血性脑卒中大鼠的神经功能恢复,这可能与其下调IP区域PTEN表达水平相关。

《动物分子遗传标记》实验教学设计与实践

基于“新农科”动物生产类专业创新型复合畜牧人才培养的需求,将CRISPR/Cas9介导的基因敲除小鼠模型引入动物分子遗传标记实验课程中,设计了基因缺失分子标记检测与分析实验,采用基于PBL的混合式教学模式,学生能系统掌握基因组DNA提取、PCR扩增技术、琼脂糖凝胶电泳分析、基因型判定等相关理论和实验技术,将多门专业课程的实践环节有机结合,促进了学生理论知识与实验技能的融会贯通,激发了学生的学习热情,提升了专业认同感,培养了综合素质和创新能力。

miR-21低表达对垂体瘤细胞系RC-4BC增殖、凋亡的影响及与PTEN靶向关系

目的观察微小RNA-21(miR-21)低表达对垂体瘤细胞系RC-4BC增殖、凋亡的影响,并分析其与第10号染色体丢失的张力蛋白同源磷酸酶基因(PTEN)的靶向关系。方法取对数生长期的RC-4BC细胞分为两组,沉默组转染miR-21抑制物miR-21 inhibitor,阴性对照组转染抑制物阴性对照NC-inhibitor,采用RT-PCR法检测miR-21、第10号染色体丢失的张力蛋白同源磷酸酶基因(PTEN)mRNA,采用CCK8实验观察两组细胞增殖能力(以OD值表示),采用平板克隆实验观察两组细胞集落形成能力(以集落形成数表示),采用流式细胞术观察两组细胞凋亡率并观察细胞周期分布情况。收集RC-4BC细胞制备单细胞悬液,分别将miR-21 mimics或NC-mimics与PTEN-WT或PTEN-MUT共转染至RC-4BC细胞,转染后细胞标记为miR-21 mimics+PTEN-WT组、NC-mimics+PTEN-WT组、miR-21 mimics+PTEN-MUT组、NC-mimics+PTEN-MUT组,采用双荧光素酶报告基因实验验证miR-21与PTEN的靶向关系。结果沉默组RC-4BC细胞中miR-21、PTEN mRNA相对表达量分别为0.30±0.08、2.89±0.14,阴性对照组RC-4BC细胞中miR-21、PTEN mRNA相对表达量分别为1.01±0.02、0.99±0.03,两组相比,P均<0.05。沉默组RC-4BC细胞24 h、48 h、72 h时OD值均低于阴性对照组(P均<0.05)。沉默组RC-4BC细胞集落形成数低于阴性对照组(P<0.05)。沉默组RC-4BC细胞凋亡率高于阴性对照组(P<0.05)。沉默组RC-4BC细胞G0/G1期占比65.65%±7.82%、S期占比19.25%±3.70%,阴性对照组RC-4BC细胞G0/G1期占比45.62%±5.03%、S期占比35.72%±4.67%,两组相比,P均<0.05。miR-21 mimics+PTEN-WT组、NC-mimics+PTEN-WT组、miR-21 mimics+PTEN-MUT组、NC-mimics+PTEN-MUT组细胞的相对荧光素酶活性分别为0.39±0.07、1.02±0.03、1.01±0.04、1.00±0.03,其中miR-21 mimics+PTEN-WT组相对荧光素酶活性与其他各组相比,P均<0.05。结论沉默miR-21能够移至垂体瘤细胞系RC-4BC的增殖、促进其凋亡,其机制可能与靶向调控PTEN基因有关。