ArticleOncoTargets and therapy2020
Histamine H3 Receptor Promotes Cell Survival via Regulating PKA/CREB/CDKN1A Signal Pathway in Hepatocellular Carcinoma.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Targeting histamine signaling: repurposing antihistamines for cancer chemotherapy and immunotherapy.Archives of pharmacal research · 2026Review
- Synthesis and Biological Activity of Novel Aromatic Aminopropyl Lactams in Two Cancer Cell Models.ChemMedChem · 2026Article
- Biological functions of tsRNAs and research advances in human disease.Biochemistry and biophysics reports · 2026Review
- Stress-induced β cell early senescence confers protection against type 1 diabetes.Cell metabolism · 2023Article
- Current and novel approaches in the pharmacological treatment of hepatocellular carcinoma.World journal of gastroenterology · 2023Review
- Exploring the role of mast cells in the progression of liver disease.Frontiers in physiology · 2022Review
- Mast cells in liver disease progression: An update on current studies and implications.Hepatology (Baltimore, Md.) · 2022Review
- Evaluation of the Differences in the Expression of Biogenic Amine-Related mRNAs and Proteins in Endometrioid Endometrial Cancer.Journal of clinical medicine · 2021Article
- Inhibition of CSRP2 Promotes Leukemia Cell Proliferation and Correlates with Relapse in Adults with Acute Myeloid Leukemia.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe histamine H3 receptor (HRH3) is mainly expressed in areas of the brain involved in the regulation of the release of various neurotransmitters. Recent studies have shown that HRH3 expression is increased in several types of carcinomas. However, the functional roles and underlying molecular mechanism by which HRH3 regulates cell survival in hepatocellular carcinoma (HCC) remain unknown.
methodsThe mRNA and protein expression level of target genes were evaluated by qRT-PCR, Western blot and immunohistochemistry, respectively. Cell viability and cell proliferation activity were assessed by MTS assay and EdU incorporation assay. Cell apoptosis and cell cycle were assessed by flow cytometry analysis. A xenograft mouse model was constructed to investigate the effect of HRH3 on tumor growth in vivo.
resultsOur results indicated that HRH3 was significantly upregulated in HCC, which promoted cell survival by accelerating cell proliferation and inhibiting cell apoptosis. Our results also showed that HRH3 in HCC downregulated the expression of cyclin-dependent kinase inhibitor p21 (CDKN1A) to promote G1-S phase transition by inactivating the cAMP/PKA/CREB pathway, which finally contributed to the malignant growth of HCC.
conclusionOur findings indicated that HRH3 functioned in promoting HCC survival by inactivating the cAMP/PKA/CREB pathway to downregulate CDKN1A expression. Thus, HRH3 might serve as a potential therapeutic target in HCC treatment.
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