RACK1 promotes tumorigenicity of colon cancer by inducing cell autophagy.

Cell Death Dis

Research Center of Carcinogenesis and Targeted Therapy, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.

Published: November 2018

AI Article Synopsis

  • * In a study with different samples, scientists found that higher levels of RACK1 were linked to worse colon cancer, meaning it could help the cancer grow and spread.
  • * RACK1 helps colon cancer cells multiply and survive by causing a process called autophagy, so blocking this process might be a way to treat colon cancer patients with high RACK1 levels.

Article Abstract

RACK1 is upregulated in the various types of human cancers, and considered to play a role in the development and progression of human cancer. However, the role and mechanism of RACK in the colon cancer are poorly understood. In this study, we detected RACK1 expression in 63 normal colonic mucosa, 60 colonic inflammatory polyps, 60 colonic adenomas, 180 colon adenocarcinomas, and 40 lymph node metastases by immunohistochemistry, and observed that RACK1 expression was progressively elevated in the carcinogenic process of human colonic epithelium, and RACK1 expressional levels were positively correlated with the malignant degree and lymph node metastasis of colon cancers, and negatively correlated with the patient survival. With a combination of loss-of-function and gain-of-function approaches, we observed that RACK1 promoted colon cancer cell proliferation, inhibited colon cancer cell apoptosis, and enhanced the anchorage-independent and xenograft growth of colon cancer cells. Moreover, we found that RACK1-induced autophagy of colon cancer cells; RACK1-induced autophagy promoted colon cancer cell proliferation and inhibited colon cancer cell apoptosis. Our data suggest that RACK1 acts as an oncogene in colon cancer, and RACK1-induced autophagy promotes proliferation and survival of colon cancer, highlighting the therapeutic potential of autophagy inhibitor in the colon cancer with high RACK1 expression.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6242835PMC
http://dx.doi.org/10.1038/s41419-018-1113-9DOI Listing

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