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Carnosic Acid Suppresses the Development of Oral Squamous Cell Carcinoma via Mitochondrial-Mediated Apoptosis.

ABSTRACT: Oral squamous cell carcinoma (OSCC) predominantly consists of squamous cells and is the tumor with the highest incidence of the head and neck. Carnosic acid (CA), a natural monomer drug obtained from rosemary and salvia, shows various pharmacological effects, including of tumor development. This study aimed to assess for an effect of CA on the development of OSCC and the underlying mechanisms. In CAL27 and SCC9 cells, CA inhibited cell proliferation and migration, increased intracellular levels of reactive oxygen species (ROS) and Ca2+, decreased the mitochondrial membrane potential (MMP), and promoted apoptosis. In CAL27- and SCC9-xenotransplanted BALB/c nude mice, CA inhibited the tumor growth without affecting the body weight and tissue morphology. CA upregulated Bax, Bad, cleaved Caspase-3 and -9 levels, and the cleaved PARP1/PARP1 ratio but downregulated Bcl-2 in CA-treated OSCC cells and OSCC cells-xenotransplanted BALB/c nude mice. These results indicate that CA suppresses OSCC at least via the mitochondrial apoptotic pathway and offers this natural compound as a potential therapeutic against OSCC.

SUBMITTER: Min F

PROVIDER: S-EPMC8662526 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Reversine suppresses oral squamous cell carcinoma via cell cycle arrest and concomitantly apoptosis and autophagy.

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Project description:Oral squamous cell carcinoma (OSCC), the most common malignancy of the oral and maxillofacial region, severely affects human health. However, current treatments for OSCC commonly show only a ~60% five-year survival rate of patients with distant metastases, indicating an urgent need for targeted treatments for patients with advanced metastases. Here, we report a survival-related long non-coding RNA, CYTOR, which is highly expressed in the lesions of oral cancer patients. We found that CYTOR can promote both migration and invasion in oral cancer cells as well as the epithelial-mesenchymal transition (EMT). RNA-sequencing of CYTOR-knockdown oral cancer cells revealed that CYTOR can regulate mitochondrial respiration and RNA splicing. Mechanistically, we found that nuclear-localized CYTOR interacts with HNRNPC, resulting in stabilization of ZEB1 mRNAs by inhibiting the nondegradative ubiquitination of HNRNPC. By synthesizing CYTOR-targeting small interfering RNAs (siRNAs) encapsulated in Nanoscale Metal Organic Frameworks (NMOFs), we demonstrate the targeted suppression of CYTOR to inhibit invasion and metastasis of oral cancer cells in a nude mouse model. Cumulatively, this study reveals the potential role of the CYTOR-HNRNPC-ZEB1 axis in regulating mitochondrial metabolism and glycolysis of oral cancer cells, and illustrates the effective use of lncRNA targeting in anti-metastatic cancer therapies.

2022-01-09 | GSE193143 | GEO

Downregulation of GBAS regulates oral squamous cell carcinoma proliferation and apoptosis via the p53 signaling pathway.

Project description:Purpose: Oral squamous cell carcinoma (OSCC) is the most common and severe type of head and neck malignancy. The mechanisms by which OSCC arises depend on changes in a number of different factors and genes and the clinicopathological stage of the tumors. Better understanding the possible mechanisms of OSCC would help to identify a new target for molecular targeted therapy. The current study was focused on elucidating the significance of the glioblastoma-amplified sequence (GBAS) on malignant behaviors in OSCC, including proliferation and apoptosis. Patients and methods: In this study, we measured the levels of mRNA in OSCC and normal oral tissue samples using Affymetrix microarrays. We examined GBAS expression in OSCC tissues and the effect of GBAS knockdown on cell proliferation and apoptosis in vitro and in vivo. The mechanisms underlying GBAS were investigated. Results: In the present study, GBAS expression was substantially elevated in the majority of tested OSCC tissues. Further, knockdown of GBAS using lentiviral-delivered shRNA in cells had significant effects on cell proliferation, apoptosis and the cell cycle. A xenograft model was also used to assess the tumorigenicity of the GBAS knockdown on OSCC cells in vivo. Mechanistically, GBAS activated p53 signaling by regulating the mRNA and protein expression of CHEK1, AKT1, AKT2 and Bax. Finally, we also investigated the expression of GBAS in patients with OSCC, and the data revealed that GBAS expression was correlated with the rates of relapse and tumor grade. Conclusion: Our studies provide evidence that GBAS regulates OSCC cell proliferation and apoptosis via p53 signaling, which may be a candidate biomarker for the prognosis and treatment of OSCC.

| S-EPMC6529179 | biostudies-literature

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| S-EPMC6933408 | biostudies-literature

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