Knockdown of lncRNA HCP5 Suppresses the Progression of Colorectal Cancer by miR-299-3p/PFN1/AKT Axis
Authors Bai N, Ma Y, Zhao J, Li B
Received 28 March 2020
Accepted for publication 1 June 2020
Published 19 June 2020 Volume 2020:12 Pages 4747—4758
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Eileen O'Reilly
Ni Bai, Ying Ma, Jia Zhao, Bo Li
Department of Laboratory Medicine, The Affiliated Xi’an Centre Hospital of Xi’an Jiaotong University College of Medicine, Xi’an, Shaanxi 710003, People’s Republic of China
Correspondence: Bo Li
Department of Laboratory Medicine, The Affiliated Xi’an Centre Hospital of Xi’an Jiaotong University College of Medicine, 161 Xi Wu Road, Xi’an, Shaanxi 710003, People’s Republic of China
Background: Colorectal cancer (CRC) is one of the most common malignant tumors in the digestive system. The lncRNA HCP5 has been reported to affect the progression of tumor in several types of cancer. Here, in this research, we focus on the role and function of lncRNA HCP5 in human colorectal cancer.
Materials and Methods: Tissue samples from colorectal cancer patients were used for detecting the expression of HCP5 by qRT-PCR. Proliferation, migration, invasion and apoptotic cells were assessed by CCK-8, colony formation, transwell assays and flow cytometry in SW480 and HCT-116 cells. The interactions between miR-299-3p and HCP5 or PFN1 were analyzed and confirmed by online database and luciferase reporter assays. The changes in PFN1 and AKT proteins were measured by Western blot. In vivo experiment was used to confirm the role of HCP5 in CRC.
Results: The expression of HCP5 had a higher level in colorectal cancer samples and cells by qRT-PCR, comparing with the normal colorectal tissues and human normal colon epithelial cell. It was revealed that knockdown of HCP5 inhibited viabilities, migration and invasion, while inducing apoptosis in SW480 and HCT-116 cells. Then, HCP5 negatively regulated the expressions of miR-299-3p, which negatively regulated the expressions of PFN1 by targeting PFN1. Furthermore, miR-299-3p inhibitor could alleviate the inhibiting effect by si-HCP5 on cell process of SW480 and HCT-116 cells. In addition, the lncHCP5/miR-299-3p/PFN1 axis could affect the progression of CRC through activating the AKT signaling. Last, we confirmed that knockdown of HCP5 inhibited the progression of CRC with an in vivo experiment.
Conclusion: The experiments and analyses support our hypothesis that knockdown of lncRNA HCP5 suppresses the progression of colorectal cancer by miR-299-3p/PFN1/AKT axis.
Keywords: lncRNA HCP5, miR-299-3p, PFN1, AKT, human colorectal cancer
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