Basic Study
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Dec 15, 2022; 14(12): 2353-2366
Published online Dec 15, 2022. doi: 10.4251/wjgo.v14.i12.2353
Anti-silencing function 1B knockdown suppresses the malignant phenotype of colorectal cancer by inactivating the phosphatidylinositol 3-kinase/AKT pathway
Gen-Hua Yu, Xu-Feng Gong, Ying-Ying Peng, Jun Qian
Gen-Hua Yu, Xu-Feng Gong, Ying-Ying Peng, Department of Radiation Oncology, Zhebei Mingzhou Hospital, Huzhou 313000, Zhejiang Province, China
Jun Qian, Department of Colorectal Surgery, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Hangzhou 310022, Zhejiang Province, China
Author contributions: Yu GH, Gong XF and Qian J were involved in the conceptualization; Peng YY and Qian J contributed to the formal analysis and investigation; Yu GH and Gong XF wrote the original draft.
Supported by Huzhou Science and Technology Bureau Foundation, No. 2018GY09.
Institutional review board statement: The current study received permission from the Ethics Committee of Zhebei Mingzhou Hospital (ZBMZYYLL211028).
Institutional animal care and use committee statement: Animal experiments obtained permission from the Institutional Animal Care and Use Committee of Beijing Viewsolid Biotechnology Co., Ltd (VS212601454), which complied with the National Institutes of Health Guide for the Care and Use of Laboratory Animals as well as ARRIVE guidelines.
Informed consent statement: All subjects signed informed consents.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: All the data used to support the findings of this study are included within the article.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Corresponding author: Jun Qian, MD, PhD, Professor, Surgeon, Department of Colorectal Surgery, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), No. 1 Banshan East Road, Gongshu District, Hangzhou 310022, Zhejiang Province, China.
Received: June 29, 2022
Peer-review started: June 29, 2022
First decision: August 6, 2022
Revised: August 31, 2022
Accepted: November 4, 2022
Article in press: November 4, 2022
Published online: December 15, 2022
Research background

Colorectal cancer (CRC) is identified as a malignant gastrointestinal tumor, with high prevalence and mortality. Abundant studies have proved the important role of anti-silencing function 1B (ASF1B) in cancers, but little is known about ASF1B in CRC.

Research motivation

In order to identify the prognosis biomarker and treatment target for CRC.

Research objectives

To evaluate the role and mechanism of ASF1B in CRC.

Research methods

The mRNA expression of ASF1B was detected by quantitative real-time polymerase chain reaction. The clinical value of ASF1B for diagnosis and prognosis of CRC was assessed. The function of ASF1B was evaluated using in vitro assays and in vivo tumor formation experiments. The molecular mechanism of ASF1B on the phosphatidylinositol 3-kinase (PI3K)/AKT pathway was explored via the addition of PI3K activator.

Research results

The expression level of ASF1B was markedly increased in CRC tissues and cells, which was inversely associated with survival time of CRC patients and positively associated with tumor node metastasis stage of CRC patients. Biological functional analyses indicated that ASF1B knockdown may suppress the malignancy of CRC cells by regulating the PI3K/AKT pathway.

Research conclusions

ASF1B is highly expressed in CRC tissues and cells, showing potential as a diagnostic and prognostic biomarker for CRC. Silencing of ASF1B inactivated the PI3K/AKT pathway to inhibit CRC malignancy in vitro.

Research perspectives

Other mechanisms of ASF1B in CRC may be investigated in the future, and its application in anti-tumor therapy will be extended.