miR-31 affects colorectal cancer cells by inhibiting autophagy in cancer-associated fibroblasts
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Xiaodong Yang1,*, Xiaohui Xu1,2,*, Junjia Zhu1,*, Shuyu Zhang3, Yong Wu1, Yongyou Wu1, Kui Zhao1, Chungen Xing1, Jianping Cao3, Hong Zhu4, Ming Li3, Zhenyu Ye1, Wei Peng1
1Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China
2Department of General Surgery, The First People’s Hospital of Taicang City, Taicang Affiliated Hospital of Soochow University, Suzhou 215400, China
3School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou 215123, China
4Oncology Department, The First Affiliated Hospital of Soochow University, Suzhou 215006, China
*These authors have contributed equally to this work
Chungen Xing, email: firstname.lastname@example.org
Jianping Cao, email: email@example.com
Keywords: miR-31, colorectal cancer, CAFs, autophagy, biological behaviors
Received: October 06, 2015 Accepted: September 25, 2016 Published: October 25, 2016
Autophagy is a double-edged sword in tumor development. Recent studies have found that miRNAs have an inhibitory effect on the regulation of autophagy. It has been reported that miR-31 plays an important role in the development of colorectal cancer. However, what role miR-31 plays in colorectal cancer-associated fibroblasts (CAFs) has not been determined. In this study, we confirmed that the expression of miR-31 in CAFs was higher than in normal colorectal fibroblasts (NFs). We also found that treatment of CAFs with miR-31 mimic inhibited the expression of the autophagy-related genes Beclin-1, ATG, DRAM and LC3. In addition, we found up-regulation of miR-31 significantly affected colorectal cancer cell behaviors, including proliferation, invasion and apoptosis. Also, up-regulation of miR-31 in CAF could increase the radiosensitivity of colorectal cancer cells co-cultured with CAF. In summary, miR-31 can inhibit autophagy in colorectal CAFs, affect colorectal cancer development, and increase the radiosensitivity of colorectal cancer cells co-cultured with CAF. We hypothesize that miR-31 may become a new target of treatments for colorectal cancer.
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