Basic Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Apr 15, 2024; 16(4): 1479-1499
Published online Apr 15, 2024. doi: 10.4251/wjgo.v16.i4.1479
FAM53B promotes pancreatic ductal adenocarcinoma metastasis by regulating macrophage M2 polarization
Xuan-Zeng Pei, Min Cai, Da-Wei Jiang, Song-Hai Chen, Qing-Qing Wang, Hui-Min Lu, Yi-Fan Lu
Xuan-Zeng Pei, Min Cai, Da-Wei Jiang, Song-Hai Chen, Qing-Qing Wang, Yi-Fan Lu, Department of Hepatological Surgery, The First Hospital of Jiaxing, Jiaxing 314000, Zhejiang Province, China
Hui-Min Lu, Department of General Surgery, West China Hospital of Sichuan University, Chengdu 610044, Sichuan Province, China
Author contributions: Pei XZ wrote the manuscript; Cai M, Jiang DW, Chen SH, Wang QQ and Lu HM collected the data; Lu YF conceived and guided the study. All authors reviewed, edited, and approved the final manuscript and critically revised it for important intellectual content, gave final approval of the version to be published, and agreed to be accountable for all aspects of the work.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board at West China Hospital of Sichuan University.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the West China Hospital of Sichuan University.
Conflict-of-interest statement: The authors declare having no conflicts of interest.
Data sharing statement: Technical appendix, statistical code, and dataset available from the corresponding author at [email: luyifan927@163.com]. Participants gave informed consent for data sharing.
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 Non-Commercial (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: Yi-Fan Lu, PhD, Assistant Professor, Department of Hepatological Surgery, The First Hospital of Jiaxing, No. 1882 Zhonghuan South Road, Nanhu District, Jiaxing 314000, Zhejiang Province, China. luyifan927@163.com
Received: November 20, 2023
Peer-review started: November 20, 2023
First decision: December 26, 2023
Revised: January 8, 2024
Accepted: March 1, 2024
Article in press: March 1, 2024
Published online: April 15, 2024
Processing time: 142 Days and 20.4 Hours
Abstract
BACKGROUND

Our study investigated the role of FAM53B in regulating macrophage M2 polarization and its potential mechanisms in promoting pancreatic ductal adenocarcinoma (PDAC) metastasis.

AIM

To further investigate the role of FAM53B in regulating macrophage M2 polarization and its potential mechanism in promoting PDAC metastasis. Our goal is to determine how FAM53B affects macrophage M2 polarization and to define its underlying mechanism in PDAC metastasis.

METHODS

Cell culture and various experiments, including protein analysis, immunohistochemistry, and animal model experiments, were conducted. We compared FAM53B expression between PDAC tissues and healthy tissues and assessed the correlation of FAM53B expression with clinical features. Our study analyzed the role of FAM53B in macrophage M2 polarization in vitro by examining the expression of relevant markers. Finally, we used a murine model to study the role of FAM53B in PDAC metastasis and analyzed the potential underlying mechanisms.

RESULTS

Our research showed that there was a significant increase in FAM53B levels in PDAC tissues, which was linked to adverse tumor features. Experimental findings indicated that FAM53B can enhance macrophage M2 polarization, leading to increased anti-inflammatory factor release. The results from the mouse model further supported the role of FAM53B in PDAC metastasis, as blocking FAM53B prevented tumor cell invasion and metastasis.

CONCLUSION

FAM53B promotes PDAC metastasis by regulating macrophage M2 polarization. This discovery could lead to the development of new strategies for treating PDAC. For example, interfering with the FAM53B signaling pathway may prevent cancer spread. Our research findings also provide important information for expanding our understanding of PDAC pathogenesis.

Keywords: FAM53B; Pancreatic ductal adenocarcinoma; Tumor metastasis; Macrophage polarization

Core Tip: Our study investigates FAM53B in regulating macrophage M2 polarization and its potential mechanisms in promoting pancreatic ductal adenocarcinoma (PDAC) metastasis. Our research revealed a significant upregulation of FAM53B in PDAC tissues, which was associated with the malignant features of the tumors. Experimental findings indicated that FAM53B can enhance macrophage M2 polarization, leading to increased release of anti-inflammatory factors. Murine model results further confirmed the role of FAM53B in PDAC metastasis, as inhibiting FAM53B suppressed tumor invasion and metastasis. Therefore, FAM53B promotes PDAC metastasis by regulating macrophage M2 polarization.