Int J Biol Sci 2019; 15(12):2750-2762. doi:10.7150/ijbs.36916 This issue
1. Department of Colorectal Surgery, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China.
2. Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Chinese PLA General Hospital, Beijing, 100048, China.
3. Department of Radiation Medicine, Faculty of Naval Medicine, The Second Military Medical University, Xiangyin Road, Shanghai, 200433, China.
4. Department of Epidemiology, Faculty of Naval Medicine, The Second Military Medical University, Xiangyin Road, Shanghai, 200433, China.
* These authors contributed equally to this work.
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.
Keywords: MTERFD1, colorectal cancer, irradiation resistance, IL-6, IL-11