Ask about this productRelated genes to: INHBA Blocking Peptide
- Gene:
- INHBA NIH gene
- Name:
- inhibin subunit beta A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-04-23
Related products to: INHBA Blocking Peptide
Related articles to: INHBA Blocking Peptide
- Gastric cancer (GC) is a leading cause of cancer mortality worldwide, and dietary factors like mycotoxins play a significant role in its etiology. Zearalenone (ZEN), a widespread grain contaminant, is a suspected carcinogen; however, its molecular mechanisms in GC remain unclear. This study used an integrated systems toxicology approach to identify key targets and pathways of ZEN-induced GC and validate the findings. - Source: PubMed
Publication date: 2026/03/31
Zheng HangbinChen ShunLin GuoHuang WenxinGuo YihuiZhang HaoJin ZiyiLin JiaLin YaoChen Liwu - Pulmonary hypertension (PH) is characterized by pulmonary vascular remodeling, which ultimately leads to right heart failure. Previous studies have confirmed that DNA variations contribute to the development and progression of PH. This study aims to integrate methylation and transcriptome data to uncover key molecular networks and potential therapeutic targets for PH. - Source: PubMed
Publication date: 2026/04/11
Jin LumingJiang BochenWang XuKong MinChen BingLiu Yun - Pulmonary arterial hypertension remains a life-threatening disease despite advances in vasodilator therapy. Vascular remodeling, partly driven by pulmonary artery endothelial cell dysfunction, is accompanied by vasoactive mediators imbalance such as ET-1 (endothelin-1). Although endothelin receptor antagonists alleviate vasoconstriction, they incompletely address the remodeling process. We previously reported how endothelial-derived activin A promotes vascular remodeling, leading to the clinical development of the activin signaling inhibitor sotatercept, which improves outcomes when added to endothelin receptor antagonists. As both activin A and ET-1 originate from endothelial cells and promote remodeling, we investigated whether activin A regulates ET-1 production and activity in pulmonary arterial hypertension. - Source: PubMed
Publication date: 2026/04/02
Faizah Novia NurulRyanto Gusty Rizky TeguhKencana Sagita Mega SekarSuzuki YokoHara TetsuyaOtake HiromasaEmoto Noriaki - Head and neck squamous cell carcinoma (HNSCC) is a major health concern with considerable morbidity and mortality worldwide. Previous studies have applied single-cell sequencing to characterize the tumor microenvironment in HNSCC, providing insights into immune cell composition, stromal interactions, and malignant cell states. However, there remains a gap in analyzing lymph node metastasis (LM) and normal lymph node tissues (LN) by using single-cell RNA sequencing (scRNA-seq) analysis. We performed comparative scRNA-seq analysis on seven lymph node metastatic tissues of HNSCC patients and five non-metastatic tissues. We identified several cell types with significantly altered expression levels, such as CD8+ Tex cells, Macrophages, and Cancer-associated fibroblasts (CAFs). Tumor cells were classified into seven clusters, with cluster2 strongly linked to tumorigenesis and metastasis. Specific subsets such as CD4_Tfh_CXCL13, CD4_Treg_RPL26, CD8_teff_CREM, NK_GZMB, Macrophages_OLFML3 and macrophages_SPP1 cells were also associated with HNSCC progression and metastasis. Based on these findings, we constructed and validated a prognostic model for HNSCC using the expression of INHBA, SFRP2, SPP1, and IFI27. This model provides a tool for risk stratification and informs potential therapeutic strategies for HNSCC. - Source: PubMed
Publication date: 2026/03/16
Wei GuannanZhang GuanghaoJiang ShanLi Ce - Prostate cancer (PCa) is a leading malignancy among men, with a growing incidence and mortality rate worldwide. There is a pressing need to identify novel molecular biomarkers and therapeutic targets to improve prognosis and treatment strategies for PCa. We analyzed thrombospondin 2 (THBS2) expression patterns in PCa using The Cancer Genome Atlas (TCGA) datasets and validated findings in clinical tissues and cell lines. Functional assays, including Cell Counting Kit (CCK)-8 proliferation, flow cytometry apoptosis, wound healing, and Transwell invasion, were performed on PCa cell lines with altered THBS2 expression. Bioinformatic analyses were conducted to explore THBS2-related pathways, and protein interactions were examined via STRING and Western blot. THBS2 expression was significantly upregulated in PCa tissues and cell lines and correlated with advanced clinicopathological features and poor prognosis. Overexpression of THBS2 promoted PCa cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while inhibiting apoptosis. Mechanistically, THBS2 interacted with INHBA to activate the focal adhesion kinase (FAK)/PI3K/AKT signaling pathway, facilitating malignant progression. INHBA knockdown reversed the oncogenic effects of THBS2, indicating a synergistic interaction between THBS2 and INHBA in PCa pathogenesis. THBS2 acts as an oncogene in PCa by promoting proliferation, invasion, and EMT via the FAK/PI3K/AKT pathway in cooperation with INHBA. These findings highlight THBS2 as a promising biomarker for PCa. - Source: PubMed
Yao YifengGuo YiyangLiu ShouleiLi YaojunChen Shanmiao