Wang Y, Zhang TY, Shen YF, Shen N, Zhang ZW. TCHP regulates the proliferation and apoptosis of gastric cancer cells via AKT/BCL2 signaling pathway. World J Gastrointest Oncol 2026; 18(8): 116937 [DOI: 10.4251/wjgo.116937]
Corresponding Author of This Article
Zhi-Wei Zhang, PhD, Department of Oncology, Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Congtai District, Handan 056000, Hebei Province, China. zhangzw128@126.com
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Oncology
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research-article
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Wang Y, Zhang TY, Shen YF, Shen N, Zhang ZW. TCHP regulates the proliferation and apoptosis of gastric cancer cells via AKT/BCL2 signaling pathway. World J Gastrointest Oncol 2026; 18(8): 116937 [DOI: 10.4251/wjgo.116937]
World J Gastrointest Oncol. Aug 15, 2026; 18(8): 116937 Published online Aug 15, 2026. doi: 10.4251/wjgo.116937
TCHP regulates the proliferation and apoptosis of gastric cancer cells via AKT/BCL2 signaling pathway
Yue Wang, Ting-Yu Zhang, Yan-Feng Shen, Na Shen, Zhi-Wei Zhang
Yue Wang, Ting-Yu Zhang, School of Clinical Medicine, Hebei University of Engineering, Handan 056000, Hebei Province, China
Yan-Feng Shen, Zhi-Wei Zhang, Department of Oncology, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
Na Shen, Department of Rheumatology and Immunology, Affiliated Hospital of Hebei University of Engineering, Handan 056000, Hebei Province, China
Co-corresponding authors: Na Shen and Zhi-Wei Zhang.
Author contributions: Zhang ZW and Shen N contributed equally to this study as co-corresponding authors; Wang Y carried out the cellular experiments, was in charge of data analysis and composed the preliminary draft; Zhang TY conducted animal experiments and analyzed the results; Shen YF contributed to data interpretation and discussion; Zhang ZW and Shen N designed the experiments, provided guidance on experimental operations, and critically revised the manuscript.
Supported by Cooperative Project of the Affiliated Hospital of Hebei University of Engineering, No. KFKT2024-05; Precision Medicine Joint Cultivation Fund Project of Hebei Natural Science Foundation, No. H2021402007; Science Research Project of Hebei Education Department, No. QN2020234; Handan Key Laboratory Project of Precision Diagnosis and Treatment of Digestive Tract Cancer, No. 23313014021; and Scientific Research Project of the Administration of Traditional Chinese Medicine of Hebei Province, No. 2022149.
Institutional animal care and use committee statement: The animal study was performed according to the institutional guidelines and ethical approval was obtained from the Animal Ethics Committee of the Affiliated Hospital of Hebei University of Engineering (Approval No. IACUC-Hebeu-2025-0018).
Conflict-of-interest statement: All authors declare no competing financial or non-financial interests related to this study.
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: Data are available from the corresponding author upon reasonable request.
Corresponding author: Zhi-Wei Zhang, PhD, Department of Oncology, Affiliated Hospital of Hebei University of Engineering, No. 81 Congtai Road, Congtai District, Handan 056000, Hebei Province, China. zhangzw128@126.com
Received: November 26, 2025 Revised: January 11, 2026 Accepted: March 3, 2026 Published online: August 15, 2026 Processing time: 247 Days and 8.8 Hours
Abstract
BACKGROUND
Gastric cancer (GC) imposes a substantial global health burden because of its high incidence and mortality. Its marked heterogeneity and poor prognosis have spurred intensive research. Therefore, identifying driver genes and elucidating the molecular mechanisms underlying GC are essential for developing more effective therapeutic strategies.
AIM
To evaluate the involvement of Trichoplein (TCHP) in controlling cellular proliferation and apoptotic processes, and to elucidate the underlying molecular mechanisms with a focus on the AKT/BCL2 signaling axis.
METHODS
TCHP expression was examined in GC cell lines and a normal gastric epithelial cell line. The Cancer Genome Atlas data analysis was performed using UALCAN, and survival analyses were conducted using KM Plotter. TCHP was knocked down using shRNA lentivirus, and the effects were analyzed using CCK-8, colony formation assay, flow cytometry, and Ki67 immunofluorescence. Proteomic profiling and Western blotting were used to study apoptotic mechanisms. Tumor growth and histopathological changes were assessed using a nude mice subcutaneous xenograft model.
RESULTS
Both in vitro experiments and analyses comparing tumor tissues with adjacent normal tissues showed increased TCHP expression in GC, and higher TCHP expression was significantly associated with poorer survival. TCHP knockdown markedly inhibited GC cell proliferation. In GC cells, reducing TCHP expression caused G1 phase accumulation and facilitated apoptotic progression. Proteomic profiling suggested that TCHP-associated changes were enriched in apoptosis-related pathways, and further pathway analysis highlighted PI3K-AKT signaling. Mechanistically, TCHP knockdown suppressed AKT/BCL2 signaling, inhibited tumor growth, and enhanced apoptosis. In vivo, TCHP knockdown significantly reduced tumor growth in xenograft models.
CONCLUSION
TCHP functions to facilitate proliferation and suppress apoptosis in GC cells through the AKT/BCL2 axis; thus, TCHP is suggested to be a promising therapeutic target for GC.
Core Tip: The function and molecular mechanism of Trichoplein (TCHP) are poorly understood in gastric cancer (GC). This study investigated the role of the centrosomal protein TCHP in GC progression. TCHP was highly expressed in GC cells, and it significantly inhibited cell proliferation, arrested the cell cycle at G1 phase, and promoted apoptosis. Proteomic analysis revealed that TCHP influenced apoptosis via AKT/BCL2 pathway. In vivo experiments further confirmed that TCHP knockdown suppressed tumor growth. These results demonstrate that TCHP promotes GC proliferation and inhibits apoptosis by activating the AKT/BCL2 pathway, suggesting its potential as a therapeutic target in GC.
