INHBA (Inhibin, beta A)

This process activates the mitochondrial GSH-GPX4 axis, thereby inhibiting mitochondrial ferroptosis. Through these two mechanisms, INHBA ultimately promotes the malignant progression of colorectal cancer.

INHBA promotes gemcitabine resistance in PC by stabilizing CTPS1 and enhancing pyrimidine metabolism, making it a potential target for chemosensitization in PC.

Research findings indicate that the INHBA gene plays a role in both carcinogenesis and prognosis. As such, it may have the potential utility as a biomarker or therapeutic target in the treatment of malignant tumors.

In conclusion, SPI1 induces the macrophage recruitment and M2 polarization by transcriptionally regulating INHBA to activating the TGF-β signaling, thereby upregulating CCL2 expression and then contributing to GC cell malignant progression. Targeting SPI1/INHBA/CCL2 axis might be a promising therapeutic strategy for GC and potentially used for cancer immunotherapy.

The KEGG pathway analysis revealed that INHBA and its interacting proteins are involved in several pathways, including TGF-beta signaling, Signalling pathways regulating pluripotency of stem cells, colorectal cancer, pancreatic cancer, AGE-RAGE signaling, and so on as major pathways. These findings demonstrate that INHBA could serve as a potential biomarker therapeutic target for GI tract cancer.

Gefitinib treatment affected NSCLC resistant cells...Both INHBA silencing and X-ray treatment inhibited EMT development. This study demonstrated that INHBA silencing ameliorates EGFR-TKI resistance and enhances the therapeutic effect of radiotherapy in NSCLC.

In conclusion, INHBA may serve a pivotal role in promoting the aggressive phenotype of TC cells through modulating the RhoA/LIMK/cofilin signaling axis. These findings highlight INHBA as a potential biomarker and therapeutic target for the management of aggressive TC.

INHBA expression is elevated within EOC, correlating with worse survival, with activin protein levels correlating with specific immune infiltration. Our findings suggest that activin-A may play a role in suppressing anti-tumor immunity in EOC, highlighting its potential as a therapeutic target.

Furthermore, the activin A-specific antibody garetosmab improved anti-tumor immunity and its combination with the anti-PD-L1 antibody atezolizumab showed a superior therapeutic effect to monotherapy with garetosmab or atezolizumab. We demonstrate that INHBA and activin A are involved in anti-tumor immunity by inhibiting the IFN-γ signaling pathway, which can be considered as potential targets to improve the responsive rate of PD-1/PD-L1 blockade.

Thus, these findings highlight the importance of INHBA and PELATON in driving CRC progression, suggesting their potential utility as diagnostic and prognostic biomarkers. By integrating computational predictions with experimental validations, this research enhances our understanding of CRC pathogenesis and uncovers prospects for personalized therapeutic interventions.

Moreover, JunB regulates tail regeneration via FGF signaling, while InhibinβA likely acts through different mechanisms. These results demonstrate that the cooperation of injury-induced InhibinβA and JunB is critical for regenerative cell proliferation, which is necessary for re-outgrowth of regenerating Xenopus tadpole tails.

Our results indicate that the upregulation of INHBA is tumor-promoting. We propose INHBA as an attractive therapeutic target for the treatment of INHBA-enriched tumors in HPV-negative OPSCC patients to ameliorate prognosis.