ArticleDigestive diseases and sciences2011
Helicobacter pylori VacA reduces the cellular expression of STAT3 and pro-survival Bcl-2 family proteins, Bcl-2 and Bcl-XL, leading to apoptosis in gastric epithelial cells.
Article in Digestive diseases and sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Helicobacter pylori cagA status and gastric mucosa-associated lymphoid tissue lymphoma: a systematic review and meta-analysis.Journal of health, population, and nutrition · 2022Pooled it
- The dual role of gastric microbiota dysbiosis in gastric cancer progression and therapy.International journal of clinical oncology · 2026Review
- Helicobacter pylori VacA modulates TRAF1-mediated 4-1BB/NF-kappaB axis to induce host apoptosis and chronic inflammatory damage.Molecular medicine (Cambridge, Mass.) · 2025Article
- Multifaceted roles of microbiota-derived deoxycholic acid in gastrointestinal cancers: from barrier disruption to therapeutic implications.Human cell · 2025Review
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Programmed cell death and melatonin: A comprehensive review.Functional & integrative genomics · 2024Review
- Listeria-vectored cervical cancer vaccine candidate strains reduce MDSCs via the JAK-STAT signaling pathway.BMC biology · 2024Article
- There Are No Insurmountable Barriers: Passage of theMembranes · 2023Review
- The inhibitory role of stigmasterol on tumor growth by inducing apoptosis in Balb/c mouse with spontaneous breast tumor (SMMT).BMC pharmacology & toxicology · 2022Article
- The Pathogenesis and Therapeutic Approaches of Diabetic Neuropathy in the Retina.International journal of molecular sciences · 2021Review
- Role of the Gastric Microbiome in Gastric Cancer: From Carcinogenesis to Treatment.Frontiers in microbiology · 2021Review
- Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins.Nature reviews. Molecular cell biology · 2019Review
- Review
- Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells.Oncotarget · 2017Article
- Review
- Cortactin Mediates Apoptosis of Gastric Epithelial Cells Induced by VacA Protein of Helicobacter pylori.Digestive diseases and sciences · 2016Article
- Regulation of Noxa-mediated apoptosis in Helicobacter pylori-infected gastric epithelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Association between Virulence Factors and TRAF1/4-1BB/Bcl-xL Expression in Gastric Mucosa Infected with Helicobacter pylori.Gastroenterology research and practice · 2015Article
- Helicobacter pylori membrane vesicles stimulate innate pro- and anti-inflammatory responses and induce apoptosis in Jurkat T cells.Infection and immunity · 2014Article
- Rapamycin induces autophagy in the melanoma cell line M14 via regulation of the expression levels of Bcl-2 and Bax.Oncology letters · 2013Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHelicobacter pylori vacuolating cytotoxin, VacA, stimulates apoptosis via a mitochondria-dependent pathway. VacA induces apoptosis via activation of the pro-apoptotic B-cell lymphoma (Bcl)-2 family proteins, Bcl-2-associated X protein (Bax) and Bcl-2 homologous antagonist/killer (Bak), while the implication of such pro-survival Bcl-2 family members as Bcl-2 and Bcl-XL in the VacA-induced apoptosis remains unknown. Signal transduction and activator of transcription 3 (STAT3) is a pivotal transcription factor that upregulates Bcl-2 and Bcl-XL.
aimsThis study was conducted to elicit the implication of STAT3 and pro-survival Bcl-2 and Bcl-XL in the intrinsic apoptosis.
methodsImmunoblot and reverse transcriptase real-time polymerase chain reaction (RT-PCR) were employed to assess the cellular expression of STAT3, Bcl-2, and Bcl-XL in response to purified VacA in gastric adenocarcinoma cell lines. VacA-induced apoptosis was quantitated morphologically following knockdown by each specific small interfering RNA (siRNA) or in the presence of pharmacological inhibitors.
resultsVacA reduced STAT3, Bcl-2, and Bcl-XL expression in a dose-dependent manner. Knockdown of STAT3, Bcl-2, and Bcl-XL by siRNA induced apoptosis to a similar extent in the case of sufficient VacA inoculation. The VacA-mediated reduction of STAT3 expression was independent of cellular vacuolization, since a vacuolar-type ATPase inhibitor, bafilomycin A1, did not inhibit VacA-induced reduction of STAT3, Bcl-2, and Bcl-XL expression. Instead, a c-JUN NH2-terminal kinase (JNK) inhibitor, SP600125, restored the VacA-induced reduction of STAT3 expression to the basal level.
conclusionsVacA-induced apoptosis may be, in part, implicated in the reduction of STAT3 linking to the downregulation of Bcl-2 and Bcl-XL, in association with JNK activity.
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20927590What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.