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Journal of Shanghai University >

2018 , Vol. 24 >Issue 1: 134 - 141

DOI: https://doi.org/10.12066/j.issn.1007-2861.1771

Research Articles

Effects of ABL silencing combined with TRAIL and DOX on apoptosis of colorectal cancer HT29 cells

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  • 1. School of Life Sciences, Shanghai University, Shanghai 200444, China
    2. Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Suzhou 215123, Jiangsu, China

Received date: 2016-04-09

  Online published: 2018-03-05

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Abstract

To investigate the effects of Abelson (ABL) tyrosine kinase silencing combined with tumor necrosis factor related apoptosis-inducing ligand (TRAIL) and doxorubicin (DOX) on apoptosis of human colon cancer cell line HT29. ABL was stably knocked down in HT29 cells using lent ivirus particles. The expression level was verified by Western blot. Cell proliferation and drug toxicity was detected by cell count kit 8 (CCK8) assay. Cell apoptosis was detected by flow cytometry. The expression level PARP1 and cleaved-caspase3 were determined by Western blot. The results showed that cell viability was reduced after treatment of TRAIL or DOX. Combination therapy can induce apoptosis rate at a lower dose. The colon cancer cell proliferation was inhibited by ABL gene silencing. However, apoptosis induced by TRAIL was inhibited, and the synergistic apoptotic effect of TRAIL and DOX on HT29 cell was also inhibited. Combination treatment can significantly induce HT29 cell apoptosis. Although ABL silencing can inhibit cell proliferation, the synergistic apoptotic effect of TRAIL and DOX on colorectal cancer HT29 cell was still inhibited by ABL silencing.

Key words： colon carcinoma; Abelson (ABL); gene silencing; tumor necrosis factor related apoptosis inducing ligand (TRAIL); doxorubicin (DOX); apoptosis

Cite this article

LI Yuyu, JIN Youxin, XU Zhongjuan, ZHANG Shumang, SUO Guangli . Effects of ABL silencing combined with TRAIL and DOX on apoptosis of colorectal cancer HT29 cells[J]. Journal of Shanghai University, 2018 , 24(1) : 134 -141 . DOI: 10.12066/j.issn.1007-2861.1771

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