Lentivirus-mediated short hairpin RNA interference of CENPK inhibits growth of colorectal cancer cells with overexpression of Cullin 4A

doi:10.3748/wjg.v28.i37.5420

Advanced Search

BPG is committed to discovery and dissemination of knowledge

Home / Archive / Volume 28, Issue 37

This Article

Peer-Review Report of This Article

CrossCheck and Google Search of This Article

Academic Rules and Norms of This Article

Supplementary Materials of This Article

Citation of this article

Corresponding Author of This Article

Research Domain of This Article

Article-Type of This Article

Open-Access Policy of This Article

Times Cited Counts in Google of This Article

Number of Hits and Downloads for This Article

Total Article Views (7318)

All Articles published online

The chart showing PDF series, WORD series, HTML series, Figures (1-9) series, Tables (1-7) series.

Item

Count

PDF

311

WORD

HTML

2730

Figures (1-9)

641

Tables (1-7)

669

Sum=4444

Publishing Process of This Article

The chart showing Browse series, Download series.

Item

Count

Browse

579

Download

2302

Sum=2881

Oct 7, 2022 (publication date) through Mar 1, 2026

Times Cited of This Article

Times Cited (4)

Journal Information of This Article

Publication Name

World Journal of Gastroenterology

ISSN

1007-9327

Publisher of This Article

Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

- Full Article with Cover (PDF)
- Full Article (XML)

Basic Study

World J Gastroenterol. Oct 7, 2022; 28(37): 5420-5443
Published online Oct 7, 2022. doi: 10.3748/wjg.v28.i37.5420

Lentivirus-mediated short hairpin RNA interference of CENPK inhibits growth of colorectal cancer cells with overexpression of Cullin 4A

Xin-Lin Wu, Lin Shi, Zhen Zhang, Zhi-Wen Yang, Guo-Sheng Xing, Yong-Xiang Ma, Xuefeng Xuefeng, Yi-Ru Han, Xian Li

Xian Li, Clinical Medical Research Center, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, Inner Mongolia Autonomous Region, China

Yi-Ru Han, Xuefeng Xuefeng, Yong-Xiang Ma, Guo-Sheng Xing, Zhi-Wen Yang, Zhen Zhang, Xin-Lin Wu, Department of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, Inner Mongolia Autonomous Region, China

Lin Shi, Department of Pathology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, Inner Mongolia Autonomous Region, China

Author contributions: Wu XL analyzed and interpreted the patient data; Han YR, XueFeng X, Ma YX, Xing GS, Yang ZW, Zhang Z, and Shi L did the experiments; Li X was a major contributor in writing the manuscript. All the authors read and approved the final manuscript.

Supported by the National Natural Science Foundation of China, No. 81860416 and No. 22168028; Inner Mongolia Autonomous Region Grassland Talent Innovation Talent Team Fund, No. 2019; and Inner Mongolia Natural Science Fund, No. 2021MS02005.

Institutional review board statement: The study was reviewed and approved by the Ethics Committee of The Affiliated Hospital of Inner Mongolia Medical University Institutional Review Board (Approval No. WZ 2021045).

Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.

Data sharing statement: No additional data are available.

Corresponding author: Xin-Lin Wu, Doctor, Chief Doctor, Department of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, No. 1 North Street, Hohhot 010050, Inner Mongolia Autonomous Region, China. wuxinlin@126.com

Received: November 22, 2021
Peer-review started: November 22, 2021
First decision: January 11, 2022
Revised: January 24, 2022
Accepted: September 12, 2022
Article in press: September 12, 2022
Published online: October 7, 2022
Processing time: 311 Days and 9 Hours

ARTICLE HIGHLIGHTS

Research background

Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. Immunohistochemistry has found high expression of centromere protein (CENPK) in CRC. However, the role of CENPK in the progression of CRC is not well characterized.

Research motivation

To explore the role of Cullin (CUL)4A expression and lentivirus-mediated transfection with short hairpin RNA (shRNA) for CENPK in CRC.

Research objectives

We performed a series of in vitro experiments, such as quantitative polymerase chain reaction (qPCR), western blot, MTT assay, and flow cytometry, to evaluate the knockdown behavior of CENPK and overexpression of CUL4A in RKO and HCT 116 CRC cells.

Research methods

We identified CENPK as a potential new oncogene for CRC based on bioinformatics analysis. In vitro experiments verified the function of this gene. We investigated the expression of CENPK in RKO and HCT 116 cells using virus infection and analyzed datasets from qPCR, western blot, and flow cytometry. The effect of RKO cells infected with virus on tumor growth was evaluated in vivo using quantitative analysis of fluorescence imaging.

Research results

The downstream genes FBX32, CUL4A, and YAP1 were examined to evaluate the regulatory action of CENPK in RKO cells. Significantly delayed xenograft emergence, slower growth, and lower final tumor weight and volume were observed in the RKO and HCT 116 with lentivirus-mediated shRNA interference of CENPK. Interference of CENPK inhibited the proliferation rate of RKO cells in vitro and in vivo. The shRNA interference of CENPK inhibited the proliferation of RKO and HCT 116 cells, and overexpression of CUL4A gene responded to RKO and HCT 116 cells with CENPK silencing.

Research conclusions

Our findings indicate a potential role of CENPK in promoting tumor proliferation, and it may serve as a novel diagnostic and prognostic biomarker in patients with CRC.

Research perspectives

An investigation for lentivirus-mediated transfection with shRNA for CENPK and overexpression of CUL4A demonstrated major regulatory roles in CRC. Further analysis is required to achieve a more comprehensive understanding of CRC diagnosis and therapy.