刺芒柄花素抑制胶质瘤细胞的增殖和迁移

目的:探讨刺芒柄花素对胶质瘤细胞增殖和迁移作用。方法:通过MTT实验检测刺芒柄花素对胶质瘤细胞（U87和U251）增殖的影响。用流式细胞仪检测刺芒柄花素对U87细胞周期的作用。通过Western blot实验和Real time PCR实验检测刺芒柄花素对Cyclin D1的作用。Transwell实验检测刺芒柄花素对U87细胞迁移的影响。Western blot实验和Real time PCR实验检测刺芒柄花素对MMP2/9的作用。结果:10 μmol/L和20 μmol/L刺芒柄花素对细胞作用24 h 后对U87细胞增殖抑制率分别是（26.74±4.26）%和（34.74±2.40）%;对U251细胞增殖的抑制率分别为（10.14±9.80）%和（27.16±9.21）%。流式实验指出刺芒柄花素对U87细胞的G1-S期具有阻滞作用。Western blot和Real time PCR实验指出刺芒柄花素可以通过抑制Cyclin D1的表达来抑制U87细胞的增殖。接下来实验发现刺芒柄花素通过抑制MMP2/9来抑制U87细胞迁移。结论:刺芒柄花素可以通过抑制Cyclin D1和MMP2/9来抑制胶质瘤细胞的增殖和迁移。     

Trastuzumab联合丁酸钠对人乳腺癌细胞株SKBR3细胞增殖和p27Kip1表达的影响

目的:观察组蛋白去乙酰化酶抑制剂(HDACIs)丁酸钠(NaB)及曲妥珠单抗Trastuzumab对人乳腺癌细胞株SKBR3细胞增殖、细胞周期及细胞凋亡的影响,探讨NaB及Trastuzumab调控乳腺癌细胞增殖的分子机制.方法:乳腺癌SKBR3细胞经NaB、Trastuzumab单独或联合作用后,MTT法检测细胞增殖情况,流式细胞仪分析细胞周期分布及细胞凋亡,Western Blot方法检测p27Kip1的表达.结果:NaB单独用药显著抑制SKBR3细胞增殖,促进细胞G0/G1期阻滞,增加细胞凋亡和p27Kip1蛋白的表达,P<0.05;20 μg/mL Trastuzumab单独用药,对细胞有增殖抑制和细胞周期阻滞作用(P<0.05),但对细胞凋亡及p27Kip1蛋白表达无明显影响,P>0.05.Trastuzumab可协助NaB 增加对SKBR3的抗肿瘤作用及p27Kip1蛋白表达,P<0.05.结论:Trastuzumab联合NaB抑制乳腺癌细胞的增殖,促进细胞周期阻滞及细胞凋亡的发生,以上过程可能是通过增加p27Kip1的蛋白表达来实现.     

Trastuzumab联合丁酸钠对人乳腺癌细胞株SKBR3细胞增殖和p27~（Kip1）表达的影响

目的：观察组蛋白去乙酰化酶抑制剂（HDACIs）丁酸钠（NaB）及曲妥珠单抗Trastuzumab对人乳腺癌细胞株SKBR3细胞增殖、细胞周期及细胞凋亡的影响,探讨NaB及Trastuzumab调控乳腺癌细胞增殖的分子机制。方法：乳腺癌SKBR3细胞经NaB、Trastuzumab单独或联合作用后,MTT法检测细胞增殖情况,流式细胞仪分析细胞周期分布及细胞凋亡,Western Blot方法检测p27Kip1的表达。结果：NaB单独用药显著抑制SKBR3细胞增殖,促进细胞G0/G1期阻滞,增加细胞凋亡和p27Kip1蛋白的表达,P〈0.05;20μg/mL Trastuzumab单独用药,对细胞有增殖抑制和细胞周期阻滞作用（P〈0.05）,但对细胞凋亡及p27Kip1蛋白表达无明显影响,P〉0.05。Trastuzumab可协助NaB增加对SKBR3的抗肿瘤作用及p27Kip1蛋白表达,P〈0.05。结论：Trastuzumab联合NaB抑制乳腺癌细胞的增殖,促进细胞周期阻滞及细胞凋亡的发生,以上过程可能是通过增加p27Kip1的蛋白表达来实现。     

Genistein对人卵巢癌细胞系3AO抑制增殖和促进凋亡的作用及机制探讨

目的 研究genistein对人卵巢癌细胞系3AO抑制增殖和促进凋亡的作用，探讨其抗癌作用的机制。方法 应用MTT法检测genistein对3AO的生长抑制作用，电镜观察凋亡细胞及凋亡小体，FCM分析细胞周期及凋亡率，免疫细胞化学法检测细胞增殖凋亡调控相关蛋白的表达。结果 genistein可明显抑制3AO的增殖，且这种抑制作用呈时间及浓度依赖性。FCM分析发现genistein阻断3AO细胞生长于细胞周期的G2／M期，且24～72h可见明显亚G1峰。电镜观察到用药后凋亡细胞典型的形态学特征。免疫细胞化学结果显示，20pmol／L的genistein作用48h后，PCNA、bcl-2及Cyclin B1蛋白表达降低，而p21^WAP1/CIP1和bax及Cyclin B1蛋白表达增加。结论 genistein对卵巢癌细胞系3AO的生长有明显的呈时间及浓度依赖性的抑制作用，其阻断细胞的生长主要在细胞周期的G2／M期，且这种生长抑制作用与p21^WAF1／CIP1蛋白水平表达增加及PCNA cy-lin B1蛋白表达降低有关，且可通过下调bcl-2蛋白表达，上调bax蛋白表达诱导卵巢癌细胞凋亡。     

三氧化二砷对人肝癌细胞生长增殖的影响

目的观察三氧化二砷（As2O3）对人BEL7402肝癌细胞株的作用及其机制。方法采用MTF法检测As2O3对BEL7402细胞的生长抑制率;流式细胞仪测定经不同浓度As2O3处理后的BEL7402细胞周期及增殖细胞核抗原（PCNA）变化,同时Annexin V—FITC／PI双染法检测细胞凋亡。结果三氧化二砷可显著抑制BEL7402细胞生长,且剂量-效应关系显著（r=0．9650,P〈0．01）,半数抑制浓度（IC50）为4．93μmol／L;BEL7402经As2O3处理后可发生凋亡。As2O3能显著下调PCNA蛋白表达（P〈0．01）,并使细胞周期阻滞在G2／M期。结论三氧化二砷可有效抑制人肝癌BEL7402细胞生长增殖,其机制可能与诱导细胞凋亡、下调PCNA表达及阻滞细胞周期有关。     

叶绿酸铜钠对SMMC7721肝癌细胞抑制作用的体外实验研究

[目的]研究叶绿酸铜钠（CHL）体外抑制SMMC7721肝癌细胞的作用及机制。[方法]（1）MTT法测半数抑制浓度（IC50）并绘制生长曲线;（2）流式细胞仪观察CHL对SMMC7721细胞凋亡的诱导作用;（3）免疫组化方法检测增殖细胞核抗原（PCNA）、细胞周期素D1（Cyclin D1）、环氧化酶-2（COX-2）的表达。[结果]（1）CHL对SMMC7721细胞具有增殖抑制作用,且具有浓度和时间依赖效应;（2）CHL能诱导SMMC7721细胞G1期阻滞,通过抑制细胞生长周期、降低细胞增生速率抑制肿瘤细胞增殖;（3）CHL对SMMC7721细胞凋亡无明显诱导作用;（4）CHL能下调SMMC7721细胞PCNA和COX-2蛋白表达,并呈一定的浓度依赖性。对Cyclin D1的表达无明显影响。[结论]CHL能抑制SMMC7721细胞的生长,这种抑制作用同PCNA、COX-2表达下调及细胞G1期阻滞有关,但与细胞凋亡和Cyclin D1的表达无关。     

不同浓度洋地黄对人乳腺癌MDA-MB-231细胞增殖和凋亡的影响

目的:研究不同浓度洋地黄对体外培养的人乳腺癌细胞株MDA-MB-231增殖和凋亡的影响,并探讨其可能机制。方法:取对数生长的细胞,不同浓度洋地黄处理,MTT法观察洋地黄对MDA-MB-231细胞活性、增殖的影响;Hoechst 33342染色观察洋地黄促细胞凋亡作用,细胞色素C含量及caspase 9活性变化检测线粒体损伤程度;生长曲线法观测洋地黄对细胞增殖的影响,Western blot检测细胞周期蛋白表达。结果:高浓度的洋地黄（≥100nmol/L）引起MDA-MB-231细胞凋亡,促进细胞色素C释放,增加caspase 9活性。低浓度洋地黄（30nmol/L）不引起肿瘤细胞凋亡,但是抑制细胞增殖,抑制细胞周期素D1和细胞增殖抗原PCNA的表达,增强p21cip1蛋白的表达。结论:高浓度洋地黄通过线粒体损伤通路促进乳腺癌细胞凋亡,低浓度洋地黄通过干扰细胞周期抑制乳腺癌细胞的生长。     

水飞蓟宾抑制人乳头状甲状腺癌TPC-1细胞增殖及诱导凋亡作用的实验研究

目的:研究水飞蓟宾(Silibinin,SB)在体外对人乳头状甲状腺癌细胞株TPC-1增殖的抑制作用。方法:采用CCK-8法观察不同浓度水飞蓟宾对TPC-1细胞株增殖的抑制作用;流式细胞仪分析细胞周期及凋亡情况;Western blot检测细胞周期分布及凋亡相关蛋白的表达变化。结果:CCK-8检测发现,水飞蓟宾呈时间-剂量依赖性地抑制TPC-1细胞株的增殖,诱导细胞凋亡及G0/G1期阻滞,并伴有细胞周期调节蛋白CDK2和CDK6的表达水平降低和凋亡相关蛋白的升高。结论:水飞蓟宾具有抑制人乳头状甲状腺癌细胞株TPC-1的增殖和诱导其凋亡的作用。     

STAT3反义寡核苷酸对乳腺癌MCF-7细胞增殖和凋亡的影响

目的探讨STAT3反义寡核苷酸的抗肿瘤机制,为乳腺癌的基因治疗提供新的实验依据。方法应用阳离子脂质体介导STAT3反义寡核苷酸转染乳腺癌MCF-7细胞,在倒置显微镜下观察细胞生长情况及形态变化;采用MTT比色法检测细胞增殖状态;流式细胞仪检测细胞凋亡率及细胞周期;Western blot检测STAT3总蛋白和p-STAT3蛋白的表达。结果STAT3反义核苷酸转染乳腺癌细胞后,能抑制MCF-7细胞的增殖,促进MCF-7细胞的凋亡,STAT3蛋白的表达和磷酸化水平下降,出现G1期阻滞。结论STAT3反义核苷酸能抑制MCF-7细胞的增殖,促进MCF-7细胞的凋亡,这将为乳腺癌的治疗提供新的方向。     

PCNA反义寡核苷酸抑制食管鳞癌细胞株T.Tn体外增殖活性的实验研究

背景与目的：增殖细胞核抗原（proliferation cell nuclear antigen,PCNA)在食管鳞癌患者中的高表达提示患者的预后不良。本研究拟通过基因反义封闭技术体外抑制PCNA的表达,以达到抑制肿瘤细胞恶性增殖的目的。方法：以食管鳞癌T.Tn细胞株为研究对象,采用硫代磷酸修饰的PCNA反义寡核苷酸（antisense oligodeoxynucleotide,ASODN),通过脂质体导入T.Tn细胞后,观察PCNA ASODN对T.Tn细胞癌基因表达及体外增殖活性的影响。结果：相关显微镜下观察到T.Tn细胞转染ASODN后细胞体积变小,皱缩变形的细胞较对照组明显减少。MTT法测细胞增殖活性见不同浓度ASODN均能抑制T.Tn细胞的增殖,抑制作用在24h最强,0．2μmol/L ASODN对细胞的抑制率为63．3％,时间延长抑制作用逐渐减弱。^3H-TdR掺入实验表明ASODN能有效地抑制T.Tn细胞的DNA合成。免疫组化SABC法染色提示转染ASODN后T.Tn细胞mRNA的翻译受到抑制,PCNA蛋白表达水平明显降低。FCM检测发现G0－G1期细胞含量由对照组的53．65％增至72．34％,而G2－M和S期细胞则分别从15．51％、30．84％降到9．87％、17．79％。表明PCNA ASODN转染导致PCNA促进细胞增殖的功能降低,抑制处于C0期的细胞进入S期。结论：使用人工合成的PCNA ASODN可以特异虱地抑制食管鳞癌T.Tn细胞株PCNA蛋白的表达,从而调控细胞周期,抑制细胞增殖。     

Fangchinoline Inhibits Cell Proliferation Via Akt/GSK-3beta/cyclin D1 Signaling and Induces Apoptosis in MDA-MB-231 Breast Cancer Cells

Fangchinoline (Fan) inhibits cell proliferation and induces apoptosis in several cancer cell lines. The effectsof Fan on cell growth and proliferation in breast cancer cells remain to be elucidated. Here, we show that Faninhibited cell proliferation in the MDA-MB-231 breast cancer cell line through suppression of the AKT/Gsk-3beta/cyclin D1 signaling pathway. Furthermore, Fan induced apoptosis by increasing the expression of Bax(relative to Bcl-2), active caspase 3 and cytochrome-c. Fan significantly inhibited cell proliferation of MDAMB-231 cells in a concentration and time dependent manner as determined by MTT assay. Flow cytometryanalysis demonstrated that Fan treatment of MDA-MB-231 cells resulted in cell cycle arrest at the G1 phase,which correlated with apparent downregulation of both mRNA and protein levels of both PCNA and cyclin D1.Further analysis demonstrated that Fan decreased the phosphorylation of AKT and GSK-3beta. In addition, Fanup-regulated active caspase3, cytochrome-c protein levels and the ratio of Bax/Bcl-2, accompanied by apoptosis.Taken together, these results suggest that Fan is a potential natural product for the treatment of breast cancer.     

siRNA沉默HYAL1基因表达对人乳腺癌细胞生长和增殖的影响

背景与目的：有研究证实透明质酸酶（hyaluronidase,Hyase）与人乳腺癌的恶性潜能相关。本研究拟探讨RNA干扰是否能有效抑制Hyde基因HYAL1的表达以及人乳腺癌细胞的生长和增殖。方法：体外化学合成HYAL1序列特异性双链RNA（dsRNA）,在脂质体（SiPORT Lipid）的介导下转染人乳腺癌细胞株MDA-MB-231、MDA-MB-453S、ZR-75和ZR-75-30。荧光共聚焦显微镜下观察转染效率,RT-PCR分析HYAL1 mRNA的表达,MTT测定细胞的增殖,流式细胞仪测定细胞周期。结果：（1）HYAL1-siRNA能有效地封闭HYALl基因的表达．使HYAL1 mRNA相对水平明显降低（P〈0．05）;（2）HYAL1-siRNA能明显抑制细胞增殖（P〈0．05）;（3）HYAL1-siRNA使细胞周期G0／G1期细胞百分比明显增加,S期的细胞百分比显著减少（P〈0．05）。结论：siRNA-HYAL1能有效抑制人乳腺癌细胞株HYAL1基因的表达,抑制细胞增殖,将更多的细胞阻滞在G0／G1期。     

Cell cycle kinase inhibitor expression and hypoxia-induced cell cycle arrest in human cancer cell lines

Flow cytometric analysis of fibroblasts, normal breast epithelial cells and breast or other cancer cell lines identified variation in the abilities of cell lines to undergo cell cycle arrest as a response to hypoxia. Human mammary epithelial cells (HMEC), normal fibroblasts (Hs68 and WI38), HeLa cervical carcinoma and HTB-30 breast carcinoma cells arrest in G(1)/S in response to severe hypoxia. Hep3B hepatocellular carcinoma cells did not exhibit orderly G(1)/S arrest in response to severe hypoxia. We found a general decrease in p16(INK4a) (p16) mRNA levels, with an associated decrease in p16 protein levels in both normal cells and in cancer cells, regardless of their cell cycle response to hypoxia. p27 protein levels did not correlate with the cell line's ability to enter a hypoxic G(1)/S arrest. Furthermore, cell lines that underwent G(1)/S arrest showed decreased expression of hypoxia inducible factor 1 (HIF-1alpha) and at least one member of INK4 or Sdi cell cycle kinase inhibitors families after 12-24 h of hypoxia. Conversely, Hep3B, which did not exhibit orderly hypoxia-associated G(1)/S arrest, also did not show decreased HIF-1alpha, INK4 or Sdi protein levels in hypoxia. Furthermore, Hep3B showed constitutive activating phosphorylation of Akt and inhibitory phosphorylation of GSK3beta, which was the opposite pattern to that exhibited by the cell lines showing the G(1)/S arrest phenotype. Inhibition of GSK3beta by lithium chloride treatment of HeLa cells converted the HIF-1alpha, p16 and p27 loss to levels unchanged by hypoxic exposure. Our results suggest that regulation of the cell cycle during hypoxia in either normal or cancer cells is not simply due to up-regulation of cell cycle kinase inhibitors. Furthermore, decreased protein expression of HIF-1alpha, p16 and p27 was associated with both a hypoxia-induced G(1)/S arrest phenotype and increased GSK3beta activity.     

Chalcone-3 Inhibits the Proliferation of Human Breast Cancer MDA-MB-231 Cell Line

Objective: Chalcone-3 has been shown to be cytotoxic and selective against luminal subtype breast cancer cell lines, which are suspected to occur through the mechanism of epidermal growth factor receptors (EGFR) inhibition. However, the cytotoxic effect has never been tested on cell strains from patients with triple negative breast cancer (TNBC), where EGFR expression is known to increase. This study aimed to identify the role of chalcone-3 in one of the downstream targets of EGFR as an antiproliferative agent. Methods: Chalcone-3 was examined for its effect on proliferation in human breast cancer MDA-MB-231 cell lines. The percentage of proliferation inhibition was analyzed using methyl-thiazol tetrazolium assay. Flow cytometry was used to analyze the population of cell cycle distribution and the expression of cyclin-D1 and pEGFR. Results: Chalcone-3 inhibited the proliferation of MDA-MB-231 cells in a dose and time-dependent manner with an IC50 value of 17.98±6.36 µg/mL by inducing cell cycle arrest at the G2/M phase. Flow cytometry assays showed that chalcone-3 significantly reduced the expression of pEGFR and cyclin-D1, contributing to cell cycle arrest. Conclusion: Chalcone-3 might have potential as an anti-proliferative drug to treat TNBC.     

环氧化酶-2抑制剂nimesulide对乳腺癌细胞株增生、凋亡的影响

目的 探讨环氧化酶-2抑制剂nimesulide(NIM)对雌激素受体(ER)阴性(MDA-MB．231)和阳性(MCF-7)人乳腺癌细胞株增生、凋亡的影响。方法 应用MTT比色法分析细胞生长抑制作用，流式细胞技术测定细胞周期分布和凋亡率，透射电镜观察细胞形态与超微结构，AnnexinV法检测细胞的凋亡。结果 NIM以时间、剂量依赖性方式抑制MDA-MB-231(COX-2阳性)、MCF-7(COX-2阴性)细胞生长，阻滞细胞周期于G0／G1期，诱导细胞的凋亡，MDA—MB-231细胞对NIM的作用更为敏感。NIM对COX-2表达阴性的MCF-7细胞同样具有抑制增生、诱导凋亡的作用。结论 NIM对ER阳性和ER阴性乳腺癌细胞均有抑制增生、诱导凋亡的作用。NIM的抗肿瘤作用存在环氧化酶．2依赖性与非依赖性两种途径。     

LRRC3B在非小细胞肺癌中下调并与肺癌细胞增殖和侵袭能力相关

背景与目的已有的研究表明：在许多恶性肿瘤细胞中,LRRC3B表达显著下调,被视为肿瘤抑制蛋白。然而,在非小细胞肺癌中它的表达模式和生物学作用缺乏研究。人类癌症微阵列的研究显示LR-RC3B在乳腺癌和结肠直肠癌表达下调,提示LRRC3B参与致癌作用。本研究的目的是研究LRRC3B在非小细胞肺癌中的必到状态及其与肺癌增殖、侵袭和细胞周期间的相关性,探讨LRRC3B在调控肺癌细胞增殖、侵袭及细胞周期中的作用。方法应用Western blot和Realtime RT-PCR检测LRRC3B在几株肺癌细胞系中的mRNA和蛋白表达水平。应用MTT法检测对转染LRRC3B的A549和H460细胞系细胞增殖能力变化,应用集落形成实验以及细胞侵袭实验研究LRRC3B对细胞增殖和侵袭以及细胞周期进程的作用。肺癌细胞系H3255中转染LR-RC3B siRAN验证LRRC3B对细胞的增殖以及侵袭能力和对细胞周期进程的影响。结果与正常NHBE细胞系相比,NSCLC细胞系中LRRC3B蛋白表达量显著下调,特别是H460、H358、HCC827以及A549。A549和H460细胞系转染LRRC3B后,细胞增殖和侵袭能力受到抑制。LRRC3B抑制细胞周期进程,并下调cyclin D1和MMP9的表达。H3255细胞中敲除LRRC3B,细胞增殖和侵袭能力显著增强,同时与细胞周期及侵袭能力相关的蛋白cyclin D1和MMP9表达略微上调。结论 LRRC3B在肺癌细胞系中表达下调,而上调LRRC3B则能够抑制肺癌细胞增殖和侵袭能力,并抑制细胞周期进程,可能是未来肺癌治疗的一个新靶点。     

Inhibition of cell proliferation, induction of apoptosis, reactivation of DLC1, and modulation of other gene expression by dietary flavone in breast cancer cell lines

BACKGROUND: Dietary flavone was previously shown to increase the expression of deleted in liver cancer-1 gene (DLC-1) in HT-29 colon carcinoma cell line [Herzog A, Kindermann B, Doring F, Daniel H, Wenzel U. Pleiotropic molecular effects of the pro-apoptotic dietary constituent flavone in human colon cancer cells identified by protein and mRNA expression profiling. Proteomics 2004;4:2455-64]. DLC-1 that encodes a Rho GTPase-activating protein, functions as a tumor suppressor gene and is frequently inactivated or down-regulated in several common cancers. Restoration of DLC-1 expression suppresses in vitro tumor cells proliferation and tumorigenicity in vivo. METHODS: Here, the effect of flavone was examined in several DLC-1-deficient cell lines derived from different types human cancer using assays for cell proliferation, gene expression and transfer. RESULTS: We show that exposure to 150 microM flavone increased DLC1 expression in breast but not in liver or prostate carcinoma cells or a nonmalignant breast epithelial cell line. Flavone restored the expression of DLC1 in the breast carcinoma cell lines MDA-MB-468, MDA-MB-361, and BT20 as well as in the colon carcinoma cell line HT-29 all of which are DLC-1-negative due to promoter hypermethylation. We further show that flavone inhibited cell proliferation, induced cell cycle arrest at G(2)-M, increased p21(Waf1) gene expression, and caused apoptosis. Microarray analysis of these aggressive and metastatic breast carcinoma cells revealed 29 flavone-responsive genes, among which the DNA damage-inducible GADD genes were up-regulated and the proto-oncogene STMN1 and IGFBP3 were down-regulated. CONCLUSIONS: Flavone-mediated alterations of genes that regulate tumor cell proliferation, cell cycle, and apoptosis contribute to chemopreventive and antitumoral effects of flavone. Alone or in combination with demethylating agents, flavone may be an effective adjunct to chemotherapy in preventing breast cancer metastasis.     

舒林酸对胃癌细胞株SGC7901细胞周期调控及凋亡的影响

目的观察舒林酸影响胃癌细胞株SGC7901细胞周期分布,诱导细胞凋亡,探讨其作用机制方法采用MTT比色法观察舒林酸对胃癌SGC7901细胞增殖的影响,采用流式细胞仪检测舒林酸对细胞周期分布的影响,同时结合透射电子显微镜观察舒林酸诱导SGC901细胞凋亡的作用;免疫细胞化学方法观察舒林酸对胃癌细胞周期调控蛋白cyvclinE及P21WAF/CIPI的影响结果舒林酸可抑制胃癌SGC7901细胞的增殖,改变细胞周期分布,使G-0/G1期细胞比例增高,S期比例降低,并对SGC7901细胞有促凋亡作用.上述作用具有剂量和时间依赖性(P＜0.05).舒林酸还可上调P21WAF/CIPI蛋白表达.下调cyolinE蛋白表达.结论舒林酸可改变细胞周期分布,影响细胞周期调控蛋白表达,并可诱导SGC7901细胞凋亡,从而抑制细胞增殖.     

Role of TMPRSS4 Modulation in Breast Cancer Cell Proliferation

Background: TMPRSS4 is a novel Type II transmembrane serine protease found at the surface of the cells andis involved in the development and cancer progression. However, TMPRSS4 functions in breast cancer remain poorunderstand. The present study investigated the function of TMPRSS4 in the breast cancer cells and the potentialmechanistic action underling. Materials and Methods: The lentiviral vectors causing TMPRSS4 down-regulation andover-expression were established and transfected in MDA-MB-468 and MCF-7 cells, respectively. By using the CCK-8 assay, cell proliferation was analyzed. Moreover, western blot was used to detect the expression of certain proteinsrelated to cell apoptosis (Bax and Bcl2) signaling pathway and telomere maintenance (POT1, TPP1, and UBE2D3).Cell cycle and cell apoptosis were also analyzed by using the Flow cytometry analysis. TMPRSS4 expression wasdetected at the mRNA level and protein level by performing qPCR and western blot technique, respectively. Results:TMPRSS4 expression is inhibited in stable transfected MDA-MB-468-shTMPRSS4 cells compared to the controlMDA-MB-468-NC and its expression is up-regulated in stable transfected MCF-7-TMPTSS4 compared to its controlMCF-7-NC. Moreover, TMPRSS4 silencing in breast cancer reduces cells proliferation by promoting cell cycle arrestin G2/M phase, cell apoptosis, and telomere maintenance impairment while the TMPRSS4 overexpression increasescells proliferation through cell apoptosis reduction and telomere maintenance reinforcement associated with insignificantchange in cell cycle progression. Conclusion: TMPRSS4 plays important roles in cancer progression and may beconsidered as a good therapeutic target for cancer gene therapy especially breast cancer.