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©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
Abelson interactor 1 splice isoform-L plays an anti-oncogenic role in colorectal carcinoma through interactions with WAVE2 and full-length Abelson interactor 1
Kun Li, Yi-Fan Peng, Jing-Zhu Guo, Mei Li, Yu Zhang, Jing-Yi Chen, Ting-Ru Lin, Xin Yu, Wei-Dong Yu
Kun Li, Mei Li, Ting-Ru Lin, Department of Central Laboratory and Institute of Clinical Molecular Biology, Peking University People’s Hospital, Beijing 100044, China
Kun Li, Yu Zhang, Jing-Yi Chen, Ting-Ru Lin, Department of Gastroenterology, Peking University People’s Hospital, Peking University, Beijing 100044, China
Yi-Fan Peng, Gastrointestinal Cancer Center, Unit III, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing 100142, China
Jing-Zhu Guo, Department of Pediatrics, Peking University People’s Hospital, Beijing 100044, China
Yu Zhang, Jing-Yi Chen, Wei-Dong Yu, Department of Central Laboratory and Institute of Clinical Molecular Biology, Peking University People's Hospital, Beijing 100044, China
Xin Yu, Department of Hepatobiliary Surgery, Peking University People’s Hospital, Beijing 100044, China
Author contributions: Li K, Peng YF, and Guo JZ contributed equally to this work and performed the majority of experiments; Li M, Zhang Y, Chen JY, Lin TR, and Yu X performed minor experiments, provided vital reagents, and were also involved in revising the manuscript; Peng YF and Yu WD designed the study, wrote the manuscript, and provided financial support; all authors read and approved the final manuscript.
Supported by National Natural Science Foundation of China, No. 30872923 and No. 81672853; and Peking University People’s Hospital Scientific Research Development Found, No. RDH2020-11.
Institutional review board statement: The study was reviewed and approved by the Peking University People’s Hospital Institutional Review Board (No. 2020-11).
Conflict-of-interest statement: The authors declare that they have no conflicts of interest to disclose.
Data sharing statement: No additional data are available.
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: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Wei-Dong Yu, PhD, Professor, Department of Central Laboratory and Institute of Clinical Molecular Biology, Peking University People's Hospital, No. 11 Xizhimen South Street, Xicheng District, Beijing 100044, China.
weidongyu@bjmu.edu.cn
Received: January 21, 2021
Peer-review started: January 21, 2021
First decision: February 9, 2021
Revised: February 17, 2021
Accepted: March 13, 2021
Article in press: March 13, 2021
Published online: April 21, 2021
Processing time: 82 Days and 21.1 Hours
ARTICLE HIGHLIGHTS
Research background
Abnormally expressed and/or phosphorylated Abelson interactor 1 (ABI1) participates in the metastasis and progression of colorectal carcinoma (CRC), but the roles of ABI1 splice isoforms (ABI1-SIs) are unknown. Exploring the roles and underlying mechanism of ABI1-SIs has important theoretical and practical significance for molecular diagnosis and targeted therapy of CRC.
Research motivation
ABI1-SIs-L (ABI1-SiL) plays an anti-oncogenic role in CRC, and it may be a potential molecular marker and therapeutic target in CRC.
Research objectives
To exploring the roles and underlying mechanism of ABI1-SiL in CRC.
Research methods
We report a set of polymerase chain reaction-based methods that can specifically measure ABI1-SiL mRNA expression and constructed an ABI-SiL overexpressing SW480 cell model. CCK8, transwell, immunoprecipitation, Western blot, and co-localization assays were used to identify the anti-oncogenic role of ABI-SiL and the underlying mechanism in CRC.
Research results
ABI-SiL had a potential anti-tumor effect in CRC. Overexpression of ABI-SiL did not affect the proliferation and invasion of SW480 cells, but can increase the surface area and migration of SW480 cells by competitively binding WAVE2 and ABI1-p65.
Research conclusions
ABI1-SiL plays an antioncogenic role in CRC cells by competitively binding WAVE2 and ABI1-p65.
Research perspectives
Targeting ABI1-SIL expression is a potential treatment for colorectal cancer metastasis.
