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ARTICLE

INHBA Promotes the Progression of Gastric Cancer by Activating MAPK Signaling Pathway via Targeting ITGA6

Guojian Zhou1,2,#, Rui Zhang1,#, Lei Nie1,#, Yi Si1, Ting Liu1, Jing Wang1, Shuangshuang Han1, Mingda Xuan1, Jia Wang3,*, Weifang Yu1,*
1 Gastrointestinal Disease Diagnosis and Treatment Center, The First Hospital of Hebei Medical University, Shijiazhuang, 050000, China
2 Gastroenterology Department, The Affiliated Hospital of Hebei University, Baoding, 071000, China
3 Department of Infectious Diseases, The First Hospital of Hebei Medical University, Shijiazhuang, 050000, China
* Corresponding Author: Jia Wang. Email: email; Weifang Yu. Email: email
# These authors contributed equally to this work
(This article belongs to the Special Issue: Identification of potential targets and biomarkers for cancers and the exploration of novel molecular mechanisms of tumorigenesis and metastasis)

Oncology Research https://doi.org/10.32604/or.2025.070333

Received 13 July 2025; Accepted 19 December 2025; Published online 14 January 2026

Abstract

Objectives: Gastric cancer (GC) is among the most prevalent malignancies worldwide, ranking as the fifth most common cancer and the fifth leading cause of cancer-related mortality. This study intends to investigate how Inhibin subunit beta A (INHBA) promotes the progression of GC by activating the mitogen-activated protein kinase (MAPK) signaling pathway via targeting Integrin alpha-6 (ITGA6). Methods: Quantitative reverse transcription-Polymerase Chain Reaction (qRT-PCR) and Immunohistochemistry (IHC) were utilised to validate the expression levels of INHBA in GC, which were subsequently correlated with the clinicopathological factors and outcomes. Cellular and animal studies were conducted to ascertain the role of INHBA in GC. RNA-sequencing (RNA-seq) and bioinformatics analysis were used to screen for the downstream target and pathway of INHBA, with Co-immunoprecipitation (Co-IP), Co-Immunofluorescent (Co-IF), Western blot (WB) and Rescue experiments validating their mechanisms of action in GC. Results: IHC and qRT–PCR analysis confirmed that GC tissues exhibited higher INHBA expression than adjacent noncancerous tissues. This elevated INHBA expression was found to be significantly associated with the incidence of tumor lesions, lymph node metastasis, and progression to higher TNM stages. Functional experiments showed that INHBA promoted GC cell proliferation and enhanced their migration and invasion in vitro while inhibiting apoptosis. Animal studies results indicated that INHBA overexpression promoted tumor growth and increased tumor weight and volume. Through a series of experiments, including RNA-seq, Co-IP, Co-IF, WB, and rescue assays, this study demonstrated that INHBA promotes GC progression by targeting ITGA6 to regulate the MAPK signaling pathway. Conclusions: INHBA/ITGA6/MAPK axis can provide new insights into GC therapy. Targeted INHBA inhibition holds promise as a therapeutic approach for GC treatment.

Keywords

Gastric cancer (GC); inhibin subunit beta A (INHBA); integrin alpha-6 (ITGA6); RNA-sequencing (RNA-seq); mitogen-activated protein kinase (MAPK)

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