Knockdown of TCTN1 Strongly Decreases Growth of Human Colon Cancer Cells.
Knockdown of TCTN1 Strongly Decreases Growth of Human Colon Cancer Cells.
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DOI：
10.12659/msm.899595
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发表时间：
2017-01-26
期刊：
影响因子：
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通讯作者：
Li K
中科院分区：
文献类型：
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作者：
Dai X;Dong M;Yu H;Xie Y;Yu Y;Cao Y;Kong Z;Zhou B;Xu Y;Yang T;Li K
构造家族成员1 （TCTN1）是构造家族成员之一，参与多种发育过程，在多种实体肿瘤中异常表达。然而，TCTN1在人类结直肠癌（CRC）中的表达和调控尚不清楚。TCTN1 mRNA的表达首先通过Oncomine微阵列数据集进行了探索。通过RNA干扰（RNAi）使TCTN1在人结直肠癌细胞系HCT116和SW1116中的表达沉默。此外，我们通过MTT、集落形成和体外流式细胞术研究TCTN1缺失对CRC细胞生长的影响。本研究荟萃分析显示，TCTN1 mRNA在结直肠癌标本中的表达明显高于正常标本。TCTN1表达下调可有效抑制细胞增殖和集落形成的能力。流式细胞术分析显示TCTN1缺失可导致细胞周期阻滞在G2/M期。此外，Annexin V/7-AAD双染色显示TCTN1沉默通过下调caspase 3和Bcl-2，上调cleaved caspase 3和PARP促进细胞凋亡。我们的研究结果表明TCTN1可能对结直肠癌细胞生长至关重要，为结直肠癌靶向治疗提供了一种新的替代方案。对这一课题的进一步研究是有必要的。
Tectonic family member 1 (TCTN1), a member of the tectonic family, is involved in several developmental processes and is aberrantly expressed in multiple solid tumors. However, the expression and regulation of TCTN1 in human colorectal cancer (CRC) is still not clear. The expression of TCTN1 mRNA was first explored by using Oncomine microarray datasets. TCTN1 expression was silenced in human CRC cell lines HCT116 and SW1116 via RNA interference (RNAi). Furthermore, we investigated the effect of TCTN1 depletion on CRC cell growth by MTT, colony formation, and flow cytometry in vitro. In this study, meta-analysis showed that the expressions of TCTN1 mRNA in CRC specimens were significantly higher than that in normal specimens. Knockdown of TCTN1 expression potently inhibited the abilities of cell proliferation and colony formation as determined. Flow cytometry analysis showed that depletion of TCTN1 could cause cell cycle arrest at the G2/M phase. In addition, Annexin V/7-AAD double-staining indicated that TCTN1 silencing promoted cell apoptosis through down-regulation of caspase 3 and Bcl-2 and upregulation of cleaved caspase 3 and PARP. Our results indicate that TCTN1 may be crucial for CRC cell growth, providing a novel alternative to target therapies of CRC. Further research on this topic is warranted.