杨世荣,白翔宇,吴 迪,韩 悦,何显力.ATAD3A在结直肠癌组织中的表达及其对细胞生长的影响[J].现代生物医学进展英文版,2020,(6):1033-1037. |
ATAD3A在结直肠癌组织中的表达及其对细胞生长的影响 |
The Expression of ATAD3A in Colorectal Cancer and Its Influence on Cell Growth |
Received:December 10, 2019 Revised:December 31, 2019 |
DOI:10.13241/j.cnki.pmb.2020.06.007 |
中文关键词: ATAD3A 结直肠癌 细胞周期 增殖 凋亡 |
英文关键词: ATAD3A Colorectal cancer Cell cycle Proliferation Apoptosis |
基金项目:国家自然科学基金国际科技合作项目(2013DFA32110) |
Author Name | Affiliation | E-mail | YANG Shi-rong | Department of General Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China State Key Laboratory of Cancer Biology, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China | yangshirong8819@163.com | BAI Xiang-yu | Pharmaceutical College of Henan University, Kaifeng, Henan, 475004, China State Key Laboratory of Cancer Biology, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China | | WU Di | Department of General Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China | | HAN Yue | Department of General Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China | | HE Xian-li | Department of General Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, 710032, China | |
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中文摘要: |
摘要 目的:探讨三磷酸腺苷酶家族蛋白3A(ATAD3A)在结直肠癌组织中的表达情况,并验证其对结直肠癌细胞RKO和HCT116生长的影响。方法:收集结直肠癌患者配对癌与癌旁组织115例,通过免疫组化方式验证ATAD3A在结直肠癌组织与癌旁的表达差异。采用慢病毒转染和si-RNA干涉的方式构建ATAD3A过表达和敲低肠癌细胞系,并采用MTS,流式检测细胞周期和细胞凋亡等方法验证ATAD3A对结直肠癌细胞系RKO和HCT116的影响。结果:ATAD3A在结直肠癌组织中表达较癌旁组织显著升高(P<0.001)。在结直肠癌细胞系RKO和HCT116中过表达ATAD3A后,细胞增殖能力明显增强,处于S期的细胞比例明显增加,而且细胞凋亡数量明显减少。反之,在上述肠癌细胞中干涉ATAD3A后,细胞增殖能力减弱,细胞大部分停滞于G1期,而且凋亡细胞数量明显增多。结论:ATAD3A在结直肠癌组织中表达升高,且ATAD3A通过促进细胞增殖、细胞周期进程和抑制细胞凋亡等方式促进肠癌细胞的生长。 |
英文摘要: |
ABSTRACT Objective: To investigate the expression of ATPase family AAA Domain-containing protein 3A(ATAD3A)in colorectal cancer (CRC), and its influence on cell growth in CRC cell lines RKO and HCT116. Methods: 115 paired CRC tissues were collected to detect the expression of ATAD3A by immunochemistry staining. Lentivirus transfection and siRNA interference were used to overexpression and knockdown ATAD3A in CRC cells, and western blot was used to determine the ATAD3A expression in these cells. Cell proliferation was measured by MTS assay. Flow cytometry was used to detect the cell cycle and apoptosis. Results: The expression of ATAD3A in CRC was significantly upregulated than adjacent normal tissues(P<0.001). Overexpression of ATAD3A in RKO and HCT116 significantly promoted cell proliferation, upregulated the S phase fractions and reduced cell apoptosis. In contrast, knockdown ATAD3A in CRC cells obviously inhibited cell proliferation, G1 phase arrest and enhanced cell apoptosis. Conclusion: ATAD3A was frequently upregulated in CRC tissues, and promoted CRC cell proliferation, advanced cell cycle procession and inhibited cell apoptosis. |
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