Circular RNA hsa_circ_000984 promotes colon cancer growth and metastasis by sponging miR-106b

// Xiao-Wu Xu 1, * , Bo-An Zheng 2, * , Zhi-Ming Hu 3 , Zhen-Yuan Qian 1 , Chao-Jie Huang 1 , Xi-Qiang Liu 3 and Wei-Ding Wu 3 1 Department of Gastrointestinal and Pancreatic Surgery, Zhejiang Provincial People's Hospital, Key Laboratory of Gastroenterology of Zhejiang Provincial People's Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, China 2 Department of Colorectal Surgery, Zhejiang Provincial People's Hospital, Hangzhou, 310014, Zhejiang, China 3 Department of Hepatobiliary-Pancreatic Surgery, Zhejiang Provincial People's Hospital, Hangzhou, 310014, Zhejiang, China * These authors have contributed equally to this work Correspondence to: Wei-Ding Wu, email: Weidingwu@126.com Xi-Qiang Liu, email: 2583749877@qq.com Keywords: circular RNA, hsa_circ_000984, colon cancer, growth, miR-106b Received: June 05, 2017 Accepted: July 30, 2017 Published: October 10, 2017 ABSTRACT Circular RNAs (circRNAs) as a novel type of noncoding RNAs (ncRNAs) are widely studied in the development of human various diseases, including cancer. Here, we found circular RNA hsa_circ_000984 encoded by the CDK6 gene was remarkably upregulated in the tissues of colorectal cancer (CRC) patients and in the CRC cell lines. Moreover, high expression level of hsa_circ_000984 was significantly associated with advanced colorectal cancer. Further analysis revealed that hsa_circ_000984 knockdown could inhibit cell proliferation, migration, invasion in vitro and tumor formation in vivo in CRC cell lines. Mechanically, we found that hsa_circ_000984 may act as a competing endogenous RNA (ceRNA) by competitively binding miR-106b and effectively upregulate the expression of CDK6 , thereby inducing a series of malignant phenotypes of tumor cells. Taken together, these observations suggest that the hsa_circ_000984 could mediate the expression of gene CDK6 by acting as a ceRNA, which may contribute to a better understanding of between the regulatory miRNA network and CRC pathogenesis.