ArticlePloS one2013
Chemoresistance to concanamycin A1 in human oral squamous cell carcinoma is attenuated by an HDAC inhibitor partly via suppression of Bcl-2 expression.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Epigenetic agents, zebularine and valproic acid, inhibit the growth of the oral squamous cell carcinoma cell line HSC4 in vitro and in vivo.Discover oncology · 2025Article
- Cleistanthin A derivative disrupts autophagy and suppresses head and neck squamous cell carcinoma progression via targeted vacuolar ATPase.Scientific reports · 2024Article
- Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Increased V-ATPase activity can lead to chemo-resistance in oral squamous cell carcinoma via autophagy induction: new insights.Medical oncology (Northwood, London, England) · 2024Review
- Identification of SPRYD4 as a tumour suppressor predicts prognosis and correlates with immune infiltration in cholangiocarcinoma.BMC cancer · 2023Article
- Anticancer activity of N-heteroaryl acetic acid salts against breast cancer; in silico and in vitro investigation.Molecular biology reports · 2022Article
- Comprehensive Analysis of a Novel Lipid Metabolism-Related Gene Signature for Predicting the Prognosis and Immune Landscape in Uterine Corpus Endometrial Carcinoma.Journal of oncology · 2022Article
- B Cell Lymphoma 2: A Potential Therapeutic Target for Cancer Therapy.International journal of molecular sciences · 2021Review
- Article
- Extracellular Vesicle-Mediated Chemoresistance in Oral Squamous Cell Carcinoma.Frontiers in molecular biosciences · 2021Review
- Dissecting the Proton Transport Pathway in Oral Squamous Cell Carcinoma: State of the Art and Theranostics Implications.International journal of molecular sciences · 2019Review
- Overcoming transporter-mediated multidrug resistance in cancer: failures and achievements of the last decades.Drug delivery and translational research · 2019Review
- The elevated activation of NFκB and AP-1 is correlated with differential regulation of Bcl-2 and associated with oral squamous cell carcinoma progression and resistance.Clinical oral investigations · 2017Article
- GLI-mediated Keratin 17 expression promotes tumor cell growth through the anti-apoptotic function in oral squamous cell carcinomas.Journal of cancer research and clinical oncology · 2017Article
- MDM2 antagonist nutlin-3a sensitizes tumors to V-ATPase inhibition.Molecular oncology · 2016Article
- Butein sensitizes HeLa cells to cisplatin through the AKT and ERK/p38 MAPK pathways by targeting FoxO3a.International journal of molecular medicine · 2015Article
- Overexpression of secretagogin inhibits cell apoptosis and induces chemoresistance in small cell lung cancer under the regulation of miR-494.Oncotarget · 2014Article
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9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
V-ATPase is involved in the acidification of the microenvironment around/in solid tumors, such as oral squamous cell carcinoma (OSCC). V-ATPase is thought to induce tumor invasion and multi-drug resistance in several malignant tumors, and it also contributes to maintaining the intracellular pH under an acidic microenvironment by inducing proton extrusion into the extracellular medium. However, there is little information regarding the effects of V-ATPase inhibitors on OSCCs. In this study, the effects of a V-ATPase inhibitor, concanamycin A1 (CMA), on the proliferation and apoptosis of OSCC were investigated in vitro. We used four OSCC cell lines, MISK81-5, SAS, HSC-4 and SQUU-B. Acridine orange staining revealed that the red fluorescence was reduced in all of the low concentration CMA-treated OSCC cells, indicating that the acidification of vesicular organelles in the OSCCs was prevented by the treatment with low-concentration of CMA. CMA treatment induced apoptosis in MISK81-5, SAS and HSC-4 cells, but not in SQUU-B cells. The p-p38 expression was not altered in CMA-treated SQUU-B cells, but their levels were increased in the other cells. The Bax/Bcl-2 ratio in CMA-treated SQUU-B cells was dramatically decreased in comparison with that in the other cell lines treated with CMA. However, when the SQUU-B cells were treated with CMA and a histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), the SQUU-B cells became more susceptible to the CMA-induced apoptosis. SAHA treatment led to a significantly decrease in the Bcl-2 expression in CMA-treated SQUU-B cells, resulting in a dramatically increased Bax/Bcl-2 ratio in comparison with that observed in the SQUU-B cells treated with CMA alone. These findings suggest that CMA could have an anti-tumor effect on OSCCs. In addition, combination of CMA with other agents, such as SAHA, could help improve the pro-apoptotic effects of CMA even in CMA-resistant OSCC cells.
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