Inhibition of ENAH gene silenced by siRNA on growth of liver cancer cell

doi:10.3877/cma.j.issn.2095-3232.2015.04.013

Abstract

Abstract:

Objective

To investigate the inhibition of ENAH gene silenced by siRNA on the growth of liver cancer cell.

Methods

ENAH-siRNA and control-siRNA were transfected to human liver cancer cell HCCLM3 using liposome Lipofectamine 2000 and ENAH-siRNA group and control-siRNA group were established. The expression of ENAH protein was detected by Western blot. Tumorigenic ability of the liver cancer cell was observed through nude mice tumorigenicity assay. Tumor volume was recorded, growth curve was drawn and survival analysis was conducted. The experimental data of two groups were compared using t test, and the survival analysis was conducted using Kaplan-Meier method and Log-rank test.

Results

The expression of ENAH protein in ENAH-siRNA group was significantly less than that in control-siRNA group. The formation time of solid tumor after inoculation in nude mice in ENAH-siRNA group was (24±3) d, which was significantly longer than (8±2) d in control-siRNA group (t=12.55, P<0.05). The median survival time of the nude mice was 64 (48~81) d in ENAH-siRNA group and was 34 (21~48) d in control-siRNA group. There was significant difference in the overall survival rate between two groups (χ²=14.33, P<0.05).

Conclusion

ENAH gene silenced by siRNA may obviously weaken the tumorigenic ability of liver cancer cell and inhibit the growth of tumor.

Key words: Liver neoplasms, Carcinogenicity tests, Growth charts, Nude mouse

Qunai Huang, Kunpeng Hu, Bo Liu, Zhicheng Yao, Zhiyong Xiong. Inhibition of ENAH gene silenced by siRNA on growth of liver cancer cell[J]. Chinese Journal of Hepatic Surgery(Electronic Edition), 2015, 04(04): 246-249.

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References 17

[1]	郭宇，陈规划．肝细胞肝癌合并肝静脉、下腔静脉及右心房癌栓的诊断与治疗[J/CD]．中华肝脏外科手术学电子杂志，2013, 2(1):53-55.
[2]	安玉玲，张婷婷，蔡常洁．西罗莫司用于治疗肝癌肝移植术后肿瘤复发患者的疗效分析[J]．器官移植，2011, 2(2):73-76.
[3]	范上达，邱宗祥，潘冬平．肝癌的综合治疗[J]．中华消化外科杂志，2011, 10(4):241-246.
[4]	Loya CM, Mcneill EM, Bao H, et al. miR-8 controls synapse structure by repression of the actin regulator enabled[J]. Development, 2014, 141(9):1864-1874.
[5]	Winkelman JD, Bilancia CG, Peifer M, et al. Ena/VASP Enabled is a highly processive actin polymerase tailored to self-assemble parallel-bundled F-actin networks with Fascin[J]. Proc Natl Acad Sci U S A, 2014, 111(11):4121-4126.
[6]	Agarwal S, Gertler FB, Balsamo M, et al. Quantitative assessment of invasive mena isoforms (Menacalc) as an independent prognostic marker in breast cancer[J]. Breast Cancer Res, 2012, 14(5):R124.
[7]	Rhim AD, Mirek ET, Aiello NM, et al. EMT and dissemination precede pancreatic tumor formation[J]. Cell, 2012, 148(1/2):349-361.
[8]	Bessède E, Staedel C, Acuña Amador LA, et al. Helicobacter pylori generates cells with cancer stem cell properties via epithelial-mesenchymal transition-like changes[J]. Oncogene, 2014, 33(32):4123-4131.
[9]	Chen XJ, Squarr AJ, Stephan R, et al. Ena/VASP proteins cooperate with the WAVE complex to regulate the actin cytoskeleton[J]. Dev Cell, 2014, 30(5):569-584.
[10]	Lim J, Thiery JP. Epithelial-mesenchymal transitions: insights from development[J]. Development, 2012, 139(19):3471-3486.
[11]	Gurzu S, Turdean S, Kovecsi A, et al. Epithelial-mesenchymal, mesenchymal-epithelial, and endothelial-mesenchymal transitions in malignant tumors: an update[J]. World J Clin Cases, 2015, 3(5):393-404.
[12]	Jain P, Spaeder MC, Donofrio MT, et al. Detection of alpha II-spectrin breakdown products in the serum of neonates with congenital heart disease[J]. Pediatr Crit Care Med, 2014, 15(3):229-235.
[13]	Huang T, Chen Z, Fang L. Curcumin inhibits LPS-induced EMT through downregulation of NF-κB-Snail signaling in breast cancer cells[J]. Oncol Rep, 2013, 29(1):117-124.
[14]	Chen Y, Yao F, Chen S, et al. Endogenous BNP attenuates cardiomyocyte hypertrophy induced by Ang II via p38 MAPK/Smad signaling[J]. Pharmazie, 2014, 69(11):833-837.
[15]	Emami H, Vucic E, Subramanian S, et al. The effect of BMS-582949, a P38 mitogen-activated protein kinase (P38 MAPK) inhibitor on arterial inflammation: a multicenter FDG-PET trial[J]. Atherosclerosis, 2015, 240(2):490-496.
[16]	Gao D, Vahdat LT, Wong S, et al. Microenvironmental regulation of epithelial-mesenchymal transitions in cancer[J]. Cancer Res, 2012, 72(19):4883-4889.
[17]	Hu K, Wang J, Yao Z, et al. Expression of cytoskeleton regulatory protein Mena in human hepatocellular carcinoma and its prognostic significance[J]. Med Oncol, 2014, 31(5):939.

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