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VPS53 Suppresses Malignant Properties in Colorectal Cancer by Inducing the Autophagy Signaling Pathway

Authors
  • Peng, Hong1
  • Zheng, Jie2
  • Su, Qiang3
  • Feng, Xueya1
  • Peng, Mingsha1
  • Gong, Lei4
  • Wu, Hong1
  • Pan, Xue5
  • 1 Department of Anorectal Surgery, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College, Nanchong, Sichuan, 637000
  • 2 Department of Anesthesiology, Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, Sichuan, 646000
  • 3 Department of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College, Nanchong Key Laboratory of Individualized Drug Therapy, Nanchong, Sichuan, 637000
  • 4 Department of Gastrointestinal Surgery, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College, Nanchong, Sichuan, 637000
  • 5 Scientific Research Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016
Type
Published Article
Journal
OncoTargets and Therapy
Publisher
Dove Medical Press
Publication Date
Oct 21, 2020
Volume
13
Pages
10667–10675
Identifiers
DOI: 10.2147/OTT.S254823
PMID: 33116643
PMCID: PMC7585861
Source
PubMed Central
Keywords
License
Green

Abstract

Background Many studies found that VPS53, one of the subunits of the golgi-associated retrograde protein (GARP) complexes, was aberrantly expressed in human diseases. Aim This study investigated the functions and molecular mechanisms of VPS53 in colorectal cancer (CRC). Methods Expression and correlation of Beclin 1 and VPS53 were analyzed by RT-qPCR and Pearson’s correlation in CRC tissues, and VPS53 expression was also determined in CRC cells. The changes of proliferation, migration, invasion, apoptosis, and autophagy of CRC cells were examined by a succession of functional experiments including CCK-8, flow cytometry, transwell assay, and electron microscopy. The levels of autophagy related proteins were evaluated by Western blotting analysis. Results RT-qPCR results found that VPS53 was downregulated in CRC tissues and cells, and Beclin 1 expression was also decreased in CRC tissues. There was a positive correlation between VPS53 and Beclin 1. Functional results showed that overexpression of VPS53 could suppress proliferation, migration, and invasion, and accelerate apoptosis and autophagy of CRC cells. Also, VPS53 could upregulate Beclin 1 and LC3BII, suggesting the inductive effect of VPS53 on CRC cell autophagy. Furthermore, it was found that the autophagy inhibitor (Inhb) could attenuate the inhibition of VPS53 on CRC progression. Conclusion VPS53 repressed CRC progression by regulating the autophagy signaling pathway, suggesting that VPS53 might be a promising therapeutic target for CRC.

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