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Transcription factor HOXC10 activates the expression of MTFR2 to regulate the proliferation, invasion and migration of colorectal cancer cells.
Molecular Medicine Reports ( IF 3.4 ) Pub Date : 2021-09-15 , DOI: 10.3892/mmr.2021.12437
Ying Xie 1 , Ran Chen 1 , Liujia Yan 1 , Zhangjun Jia 1 , Guangshu Liang 1 , Qin Wang 1
Affiliation  

HOXC10 and mitochondrial fission regulator 2 (MTFR2) have been reported to be abnormally expressed in multiple types of cancer tissues. However, the effects of HOXC10 and MTFR2 on colorectal cancer (CRC) remain poorly understood. Therefore, the present study aimed to investigate the expression of HOXC10 and MTFR2 in CRC tissues and cells, and analyze their effects on CRC cell proliferation, invasion and migration. Reverse transcription‑quantitative PCR and western blotting were used to detect the expression levels of MTFR2 and HOXC10 in tissues and cells. To investigate the association between MTFR2 and HOXC10, short hairpin RNA‑MTFR2 and overexpression vector‑HOXC10 were transfected into the cells, respectively. Furthermore, western blotting was performed to detect the expression levels of invasion‑associated proteins. The proliferation, clone formation, invasion and migration of colorectal cancer cells were in turn analyzed by the Cell Counting Kit‑8, clone formation, wound healing and Transwell assays. Japan Automotive Software Platform and Architecture software predicted the binding sites between HOXC10 and MTFR2, which was confirmed by the dual‑luciferase reporter assay and chromatin immunoprecipitation. The present study demonstrated that HOXC10 and MTFR2 mRNA and protein expression levels were significantly upregulated in CRC tissues and cells. MTFR2 knockdown significantly inhibited CRC cell proliferation, clone formation, invasion and migration. Furthermore, HOXC10 was shown to interact with MTFR2. HOXC10 overexpression was able to significantly reverse the inhibitory effects of MTFR2 knockdown on CRC cells. In conclusion, HOXC10 overexpression activated MTFR2 expression to enhance the proliferation, clone formation, invasion and migration of CRC cells.

中文翻译:

转录因子 HOXC10 激活 MTFR2 的表达以调节结直肠癌细胞的增殖、侵袭和迁移。

据报道,HOXC10 和线粒体裂变调节因子 2 (MTFR2) 在多种类型的癌组织中异常表达。然而,HOXC10 和 MTFR2 对结直肠癌 (CRC) 的影响仍然知之甚少。因此,本研究旨在研究HOXC10和MTFR2在CRC组织和细胞中的表达,并分析它们对CRC细胞增殖、侵袭和迁移的影响。采用逆转录定量 PCR 和蛋白质印迹法检测组织和细胞中 MTFR2 和 HOXC10 的表达水平。为了研究 MTFR2 和 HOXC10 之间的关联,分别将短发夹 RNA-MTFR2 和过表达载体-HOXC10 转染到细胞中。此外,进行蛋白质印迹以检测侵袭相关蛋白的表达水平。繁衍,结肠直肠癌细胞的克隆形成、侵袭和迁移依次通过细胞计数试剂盒 8、克隆形成、伤口愈合和 Transwell 分析进行分析。日本汽车软件平台和架构软件预测了 HOXC10 和 MTFR2 之间的结合位点,这通过双荧光素酶报告基因测定和染色质免疫沉淀得到证实。本研究表明,HOXC10 和 MTFR2 mRNA 和蛋白质表达水平在 CRC 组织和细胞中显着上调。MTFR2 敲低显着抑制 CRC 细胞增殖、克隆形成、侵袭和迁移。此外,HOXC10 被证明与 MTFR2 相互作用。HOXC10 过表达能够显着逆转 MTFR2 敲低对 CRC 细胞的抑制作用。综上所述,
更新日期:2021-09-15
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