Aberrant high expression level of MORC2 is a common character in multiple cancers.

Autor: Ding QS; Department of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Clinical Cancer Study Center, Zhongnan Hospital, Wuhan University, Wuhan 430071, China; Department of Gastroenterology, Institute for Gastroenterology and Hepatology, Renmin Hospital of Wuhan University, Wuhan 430060, China., Zhang L; Department of Anatomical and Cellular Pathology, State Key Laboratory of Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China., Wang BC; Department of Pathology, Zhongnan Hospital, Wuhan University, Wuhan 430071, China., Zeng Z; Department of Pathology, Renmin Hospital of Wuhan University, Wuhan 430060, China., Zou XQ; College of Biotechnology, Guilin Medical University, Guilin 541100, China., Cao PB; The State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China., Zhou GM; The State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China., Tang M; Department of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Clinical Cancer Study Center, Zhongnan Hospital, Wuhan University, Wuhan 430071, China., Wu L; Department of Gastroenterology, Institute for Gastroenterology and Hepatology, Renmin Hospital of Wuhan University, Wuhan 430060, China., Wu LL; Department of Gastroenterology, Institute for Gastroenterology and Hepatology, Renmin Hospital of Wuhan University, Wuhan 430060, China., Yu HG; Department of Gastroenterology, Institute for Gastroenterology and Hepatology, Renmin Hospital of Wuhan University, Wuhan 430060, China., Guo Y; College of Biotechnology, Guilin Medical University, Guilin 541100, China. Electronic address: guoyong74@163.com., Zhou FX; Department of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Clinical Cancer Study Center, Zhongnan Hospital, Wuhan University, Wuhan 430071, China. Electronic address: 592071015@qq.com.
Jazyk: angličtina
Zdroj: Human pathology [Hum Pathol] 2018 Jun; Vol. 76, pp. 58-67. Date of Electronic Publication: 2018 Mar 16.
DOI: 10.1016/j.humpath.2018.03.011
Abstrakt: Microrchidia 2 (MORC2) plays important roles in DNA damage repair and lipogenesis, but the clinical and functional role of MORC2 in cancer remains largely unexplored. In this study, we showed that MORC2 was widely expressed in human tissues while significantly up-regulated in most cancer types using immunohistochemical staining and analysis of messenger RNA expression profile of more than 2000 human tissue samples from 15 different organs (lung, prostate, liver, breast, brain, stomach, colon/rectum, pancreas, ovary, endometrium, skin, nasopharynx, kidney, esophagus, and bladder). We also found that the MORC2 expression level in high-grade cancer tissues was much more elevated and associated with unfavorable pathological characteristics, poor overall survival, and disease-free survival in several kinds of cancers such as non-small cell lung cancer and breast cancer. Gene set enrichment analysis was used to predict the genes modulated by MORC2, and the results showed that dysregulation of MORC2 in tumor may take part in the cell cycle regulation and genomic instability. We observed that MORC2 knockdown would arrest the cell cycle progress, and the genome of tumors with high MORC2 expression contained more point mutations and gene copy number variation, which validates our gene set enrichment analysis results. The results also showed that MORC2 knockdown would significantly inhibit the proliferation, colony forming, migration, and invasion in multiple cancer cell lines. Taken together, these results highlight the importance of MORC2 in tumorigenesis and cancer progression, and it may act as a potential diagnostic marker and therapeutic target for these diseases.
(Copyright © 2018 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: