MTERFD1 promotes cell growth and irradiation resistance in colorectal cancer by upregulating interleukin-6 and interleukin-11

MTERFD1通过上调白细胞介素-6和白细胞介素-11促进结直肠癌细胞生长和放射抗性

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作者:Xiaoshuang Liu, Xiaopeng Cao, Cong Liu, Yi Cao, Quanquan Zhao, Xiaojie Tan, Xu Li, Xiaodong Xu, Enda Yu, Hao Wang

Abstract

The role of the novel oncogene, mitochondrial transcription termination factor (MTERFD1), in human colorectal cancer (CRC) is unclear. Here, we report the role MTERFD1 in CRC. We conducted plasmid construction and transfection analyses, cell proliferation assays, apoptosis detection assays, ELISA, western blotting, and qRT-PCR using cell culture applications. MTERFD1 was upregulated in human and chemically induced mouse CRC tissues. In vitro functional assays showed that MTERFD1 overexpression promoted human CRC cell proliferation, whereas knockdown of endogenous MTERFD1 significantly enhanced apoptosis in these cells. MTERFD1 expression was positively linked to irradiation resistance in CRC cells. Furthermore, interleukin (IL)-6 and IL-11 were identified as the effector molecules of MTERFD1 in its oncogenic role and irradiation resistance in CRC cells. Our results demonstrated that MTERFD1 played an oncogenic role in CRC development and enhanced irradiation resistance by regulating IL-6 and IL-11 in CRC cells. MTERFD1 may serve as a potential prognostic and therapeutic marker for radiotherapy in CRC.

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