Effects of CHI3L1 gene silenced by siRNA on proliferation and invasion of human gallbladder carcinoma cells

doi:10.3877/cma.j.issn.2095-3232.2017.05.018

Abstract

Abstract:

Objective

To investigate the effects of CHI3L1 gene silenced by siRNA upon the proliferation and invasion of human gallbladder carcinoma cells.

Methods

The CHI3L1 gene of the human gallbladder carcinoma cell GBC-SD was silenced by slow-virus infection and siRNA interference technique (siRNA group). And negative control group (siRNA-NC group) and blank control group (GBC-SD group) were established. The cell absorbance values (A₄₅₀) among three groups were detected by CCK-8 assay. The quantity of membrane-penetrating cells was detected by Transwell cell migration and invasion assays. The cellular data among three groups were compared by one-way analysis of variance and LSD-t test.

Results

The A₄₅₀ at 24, 48, 72 h in the siRNA group was respectively 0.87±0.16, 0.47±0.21 and 0.52±0.20, significantly lower than 1.20±0.08, 1.34±0.15 and 1.58±0.21 in the GBC-SD group (LSD-t=-4.061, -8.483, -7.698; P<0.05). Transwell cell migration assay revealed that, the quantity of membrane-penetrating cells at 24 h in the siRNA group was 31.0±2.4, significantly less than 92.0±7.2 in the GBC-SD group (LSD-t=-8.126, P<0.05). Transwell cell invasion assay revealed that, the quantity of membrane-penetrating cells at 24 h in the siRNA group was 29.0±3.0, significantly less than 76.0±5.2 in the GBC-SD group (LSD-t=-7.883, P<0.05).

Conclusions

CHI3L1 gene silenced by siRNA can significantly inhibit the proliferation, migration and invasion capabilities of human gallbladder carcinoma cells.

Key words: Gallbladder neoplasms, RNA, small interfering, Neoplasm invasiveness, Cell migration assays

Liang Fu, Tao Suo, Min Li, Lujun Song. Effects of CHI3L1 gene silenced by siRNA on proliferation and invasion of human gallbladder carcinoma cells[J]. Chinese Journal of Hepatic Surgery(Electronic Edition), 2017, 06(05): 415-418.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhgzwkssxdzzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.2095-3232.2017.05.018

https://zhgzwkssxdzzz.cma-cmc.com.cn/EN/Y2017/V06/I05/415

Figures/Tables 3

References 18

[1]	Rakić M, Patrlj L, Kopljar M, et al. Gallbladder cancer[J]. Hepatobiliary Surg Nutr, 2014, 3(5):221-226.
[2]	Zhang JT, Sun W, Zhang WZ, et al. Norcantharidin inhibits tumor growth and vasculogenic mimicry of human gallbladder carcinomas by suppression of the PI3-K/MMPs/Ln-5γ2 signaling pathway[J]. BMC Cancer, 2014, 14:193.
[3]	Li M, Zhang F, Wang X, et al. Magnolol inhibits growth of gallbladder cancer cells through the p53 pathway[J]. Cancer Sci, 2015, 106(10):1341-1350.
[4]	Thöm I, Andritzky B, Schuch G, et al. Elevated pretreatment serum concentration of YKL-40-An independent prognostic biomarker for poor survival in patients with metastatic nonsmall cell lung cancer[J]. Cancer, 2010, 116(17):4114-4121.
[5]	Horbinski C, Wang G, Wiley CA. YKL-40 is directly produced by tumor cells and is inversely linked to EGFR in glioblastomas[J]. Int J Clin Exp Pathol, 2010, 3(3):226-237.
[6]	Pan JJ, Ge YS, Xu GL, et al. The expression of chitinase 3-like 1: a novel prognostic predictor for hepatocellular carcinoma[J]. J Cancer Res Clin Oncol, 2013, 139(6):1043-1054.
[7]	Libreros S, Garcia-Areas R, Shibata Y, et al. Induction of proinflammatory mediators by CHI3L1 is reduced by chitin treatment: decreased tumor metastasis in a breast cancer model[J]. Int J Cancer, 2012, 131(2):377-386.
[8]	Shao R, Cao QJ, Arenas RB, et al. Breast cancer expression of YKL-40 correlates with tumour grade, poor differentiation, and other cancer markers[J]. Br J Cancer, 2011, 105(8):1203-1209.
[9]	Johansen JS, Schultz NA, Jensen BV. Plasma YKL-40: a potential new cancer biomarker?[J]. Future Oncol, 2009, 5(7):1065-1082.
[10]	付亮，锁涛，张钰，等．几丁质酶-3样蛋白-1在胆囊癌组织中的表达及其临床意义[J]．中华实验外科杂志，2014，31(5):1114-1116.
[11]	Kawada M, Seno H, Kanda K, et al. Chitinase 3-like 1 promotes macrophage recruitment and angiogenesis in colorectal cancer[J]. Oncogene, 2012, 31(26):3111-3123.
[12]	Barone C, Basso M, Biolato M, et al. A phase II study of sunitinib in advanced hepatocellular carcinoma[J]. Dig Liver Dis, 2013, 45(8):692-698.
[13]	Marks EI, Yee NS. Molecular genetics and targeted therapeutics in biliary tract carcinoma[J]. World J Gastroenterol, 2016, 22(4):1335-1347.
[14]	Stec WJ, Rosiak K, Siejka P, et al. Cell line with endogenous EGFRvIII expression is a suitable model for research and drug development purposes[J]. Oncotarget, 2016, 7(22): 31907-31925.
[15]	Sharma KL, Rai R, Srivastava A, et al. A multigenic approach to evaluate genetic variants of PLCE1, LXRs, MMPs, TIMP, and CYP genes in gallbladder cancer predisposition[J]. Tumor Biol, 2014, 35(9): 8597-8606.
[16]	Sharma KL, Misra S, Kumar A, et al. Higher risk of matrix metalloproteinase (MMP-2, 7, 9) and tissue inhibitor of metalloproteinase (TIMP-2) genetic variants to gallbladder cancer[J]. Liver Int, 2012, 32(8):1278-1286.
[17]	陈洁盈，陈耀庭，林泽宇，等．三氧化二砷逆转低浓度索拉非尼对人肝癌细胞促迁移作用及其机制[J/CD]．中华肝脏外科手术学电子杂志，2016，5(2):114-118.
[18]	Gan HK, Cvrljevic AN, Johns TG. The epidermal growth factor receptor variant III (EGFRvIII): where wild things are altered[J]. FEBS J, 2013, 280(21): 5350-5370.

Please choose a citation manager

Content to export