Chen YL, Lin BA, Chen X, Liu XP, Huang JS. ARPC1B contributes to colorectal cancer progression and is associated with programmed death-ligand 1 expression. World J Gastroenterol 2026; 32(40): 117677 [DOI: 10.3748/wjg.117677]
Corresponding Author of This Article
Jing-Shan Huang, MD, Doctor, Department of General Surgery, The Second Affiliated Hospital of Fujian Medical University, No. 34 Zhongshan North Road, Quanzhou 362000, Fujian Province, China. hjs_mountain99@sina.com
Research Domain of This Article
Medicine, General & Internal
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research-article
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Chen YL, Lin BA, Chen X, Liu XP, Huang JS. ARPC1B contributes to colorectal cancer progression and is associated with programmed death-ligand 1 expression. World J Gastroenterol 2026; 32(40): 117677 [DOI: 10.3748/wjg.117677]
Yi-Lin Chen, Bei-An Lin, Xin Chen, Xiao-Ping Liu, Jing-Shan Huang, Department of General Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China
Author contributions: Chen YL and Huang JS conceived and designed the study; Chen YL and Lin BA performed the experiments; Chen X and Liu XP processed and analyzed the data; Huang JS wrote the manuscript; All the authors approved the manuscript.
AI contribution statement: The authors declare that no AI tools were used in the development or writing of this manuscript and take full responsibility for its integrity, accuracy, and originality.
Supported by the Natural Science Foundation of Fujian Province, No. 2022J01773.
Institutional review board statement: This study was approved by the Ethic Committee of the Second Affiliated Hospital of Fujian Medical University, No. 2022-552.
Institutional animal care and use committee statement: The animal experiments conducted in this study were overseen by Medical Ethics Committee of the Second Affiliated Hospital of Fujian Medical University, No. 2022-552.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
Corresponding author: Jing-Shan Huang, MD, Doctor, Department of General Surgery, The Second Affiliated Hospital of Fujian Medical University, No. 34 Zhongshan North Road, Quanzhou 362000, Fujian Province, China. hjs_mountain99@sina.com
Received: March 25, 2026 Revised: May 8, 2026 Accepted: June 5, 2026 Published online: October 28, 2026 Processing time: 170 Days and 21.5 Hours
Abstract
BACKGROUND
Colorectal cancer (CRC) is the third most common cancer; however, the role and mechanism of ARPC1B in CRC remain unclear.
AIM
To investigate the role of ARPC1B and its biological behavior in CRC.
METHODS
Clinical CRC samples were collected for western blotting of ARPC1B and programmed death-ligand 1 (PD-L1) expression. ARPC1B expression was further verified using The Cancer Genome Atlas and the Human Protein Atlas databases. Its oncogenic role was evaluated using cell counting kit-8, transwell assays, and flow cytometry in HT29 and SW620 cell lines in vitro. A xenograft nude mice model was established to assess tumor progression in vivo. Co-immunoprecipitation (Co-IP) assays examined the association between ARPC1B and PD-L1.
RESULTS
ARPC1B was highly expressed in CRC samples compared with paracancerous or normal samples. ARPC1B knockdown suppressed CRC cell proliferation, migration, and invasion, while promoting apoptosis in vitro. In vivo, ARPC1B knockdown inhibited tumor growth and metastasis. Additionally, PD-L1 expression decreased following ARPC1B knockdown, and Co-IP assays indicated an association between ARPC1B and PD-L1 in the CRC cells. Functional rescue experiments further showed that PD-L1 overexpression partially restored the malignant phenotype impaired by ARPC1B knockdown.
CONCLUSION
Our findings indicate that ARPC1B functions as a tumor-promoting factor in CRC and is positively associated with PD-L1 expression. The above preliminarily supports the potential involvement of ARPC1B in PD-L1-related cancer progression, though investigations into the molecular mechanisms are required.
Core Tip: ARPC1B promotes colorectal cancer proliferation and metastasis and is associated with programmed death-ligand 1 (PD-L1) expression. Suppressed tumor growth and pulmonary metastasis are observed after knocking down ARPC1B expression. This study functionally links ARPC1B to PD-L1-associated aggressive biological behaviors.
