Yu GH, Gong XF, Peng YY, Qian J. Anti-silencing function 1B knockdown suppresses the malignant phenotype of colorectal cancer by inactivating the phosphatidylinositol 3-kinase/AKT pathway. World J Gastrointest Oncol 2022; 14(12): 2353-2366 [PMID: 36568946 DOI: 10.4251/wjgo.v14.i12.2353]
Corresponding Author of This Article
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. qianj1973@aliyun.com
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Basic Study
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Yu GH, Gong XF, Peng YY, Qian J. Anti-silencing function 1B knockdown suppresses the malignant phenotype of colorectal cancer by inactivating the phosphatidylinositol 3-kinase/AKT pathway. World J Gastrointest Oncol 2022; 14(12): 2353-2366 [PMID: 36568946 DOI: 10.4251/wjgo.v14.i12.2353]
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
Jun Qian, Ying-Ying Peng, Xu-Feng Gong, Gen-Hua Yu
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 byHuzhou 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.
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. qianj1973@aliyun.com
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 Processing time: 165 Days and 23.9 Hours
ARTICLE HIGHLIGHTS
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.
