Editorial
Copyright ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Apr 28, 2023; 29(16): 2359-2368
Published online Apr 28, 2023. doi: 10.3748/wjg.v29.i16.2359
Future therapeutic implications of new molecular mechanism of colorectal cancer
Sen Lu, Cheng-You Jia, Jian-She Yang
Sen Lu, Department of Surgical Anesthesiology, First Affiliated Hospital of Anhui University of Science and Technology, Huainan 232001, Anhui Province, China
Cheng-You Jia, Jian-She Yang, Department of Nuclear Medicine and Oncology Research, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China
Author contributions: Lu S and Jia CY contributed equally to this paper; Yang JS designed the overall concept and outline of the manuscript; Lu S contributed to the discussion and design of the manuscript; Lu S, Jia CY, and Yang JS contributed to the writing and editing of the manuscript, illustrations, and review of the literature.
Supported by the National Natural Science Foundation of China, No. 72171170 and 82071964.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Jian-She Yang, MD, MM, MSc, PhD, Academic Editor, Academic Fellow, Academic Research, Full Professor, Professor, Department of Nuclear Medicine and Oncology Research, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, No. 301 Yanchang Road (Middle), Shanghai 200072, China. yangjs@impcas.ac.cn
Received: October 19, 2022
Peer-review started: October 19, 2022
First decision: December 12, 2022
Revised: December 17, 2022
Accepted: April 7, 2023
Article in press: April 7, 2023
Published online: April 28, 2023
Abstract

High incidence (10.2%) and mortality (9.2%) rates led to the ranking of colorectal cancer (CRC) as the second most malignant tumor spectrum worldwide in 2020. Treatment strategies are becoming highly dependent on the molecular characteristics of CRC. The classical theories accept two models depicting the origin of CRC: The progression of adenoma to cancer and transformation from serrated polyps to cancer. However, the molecular mechanism of CRC development is very complex. For instance, CRCs originating from laterally spreading tumors (LST) do not adhere to any of these models and exhibit extremely serious progression and poor outcomes. In this article, we present another possible pathway involved in CRC development, particularly from LST, with important molecular characteristics, which would facilitate the design of a novel strategy for targeted therapy.

Keywords: Colorectal cancer, Laterally spreading tumors, Molecular mechanism, Truncated adenomatous polyposis coli mutation, Golgi fragmentation, Cancerous mechanism

Core Tip: Although laterally spreading tumors (LST) are considered vital precancerous lesions of colorectal cancer (CRC), the mechanism mediating their transition to CRC development is unclear. Adenomatous polyposis coli (APC)-truncating mutations driven by Golgi fragmentation are very important cellular events that can abrogate the microtubule binding properties of APC. This effect reduces the stability of microtubules, impacts cell proliferation and survival, causes chromosomal instability, and increases migration. Downstream characteristics of Golgi fragmentation indicate alterations in Ataxia-telangiectasia mutated and anoctamin 5 expression, whereas their gene expression changes are significant in LST. This implies a novel pathway for CRC development from LST.