Research Papers:
Circular RNA hsa_circ_000984 promotes colon cancer growth and metastasis by sponging miR-106b
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Abstract
Xiao-Wu Xu1,*, Bo-An Zheng2,*, Zhi-Ming Hu3, Zhen-Yuan Qian1, Chao-Jie Huang1, Xi-Qiang Liu3 and Wei-Ding Wu3
1Department 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
2Department of Colorectal Surgery, Zhejiang Provincial People's Hospital, Hangzhou, 310014, Zhejiang, China
3Department 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: [email protected]
Xi-Qiang Liu, email: [email protected]
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.
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