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

Min, Feng-He; Liu, Xin; Li, Yuan; Dong, Mingyuan; Qu, Yidi; Liu, Weiwei

doi:10.3389/fonc.2021.760861

Cited by 16 publications

(11 citation statements)

References 54 publications

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“…The alteration of ROS in CNE2 cells was assessed using an ROS assay kit (Beyotime Biotechnology) as previously described (Min et al. 2021 ). Briefly, CNE2 cells were seeded in 6-well plates at a density of 3 × 10 5 cells/well and left overnight in an incubator at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

Lucialdehyde B suppresses proliferation and induces mitochondria-dependent apoptosis in nasopharyngeal carcinoma CNE2 cells

Liu

Yu²,

Chen

et al. 2023

Pharmaceutical Biology

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Context Lucialdehyde B (LB), an effective triterpenoid isolated from Ganoderma lucidum (Leyss. ex Fr.) Karst. (Polyproraceae), exerts cytotoxic activity against nasopharyngeal carcinoma CNE2 cells. Objective To investigate the antiproliferative and pro-apoptotic effects of LB on CNE2 cells and explore its underlying mechanisms. Materials and methods LB concentrations of 5–40 μg/mL were used. Cell proliferation was determined using MTT, CFSE, and colony formation assays. LB-induced apoptosis and cell cycle arrest were measured by flow cytometry after 48-h LB treatments. Fluorescence microscopy and flow cytometry were performed to measure the alteration of MMP, mPTP opening, ROS level, and Ca 2+ content in CNE2 cells. Western blotting was performed to evaluate the expression of mitochondrial apoptosis-related and Ras/ERK signaling proteins. Results IC 50 values of LB against CNE2 cells for 24, 48, and 72 h were 25.42 ± 0.87, 14.83 ± 0.93, and 11.60 ± 0.77 μg/mL, respectively. The CFSE assay showed that the cell proliferation index was 12.70 in the LB treatment group and 31.44 in the control group. LB significantly reduced clonogenic capacity, promoted cell apoptosis and induced cell cycle arrest at the G2/M phase. Our observations also revealed that LB induced ROS and calcium aggregation, opening of mPTP, MMP reduction, upregulation of mitochondrial apoptosis-related protein expression and inhibition of Ras/ERK signaling cascades. Discussion LB suppresses proliferation and induces mitochondrial-dependent apoptosis in nasopharyngeal carcinoma CNE2 cells. Conclusions LB may have a potential use as a clinical drug candidate for nasopharyngeal carcinoma treatment.

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Section: Methodsmentioning

confidence: 99%

Lucialdehyde B suppresses proliferation and induces mitochondria-dependent apoptosis in nasopharyngeal carcinoma CNE2 cells

Liu

Yu²,

Chen

et al. 2023

Pharmaceutical Biology

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“…Targeting tumor metabolism with carnosic acid represents a promising strategy to overcome drug resistance and tumor sensitization in cancer therapy. Table 3 presents a number of preclinical studies showing the antitumor activity of the сarnosic acid ( de Souza et al, 2021 ; de Oliveira et al, 2019 ; de Oliveira et al, 2016 ; Coyne and Narayanan, 2019 ; Corveloni et al, 2020 ; Liu et al, 2018a ; D'Alesio et al, 2017 ; Min et al, 2021 ; Shao et al, 2022 ; Hasei et al, 2021 ; Liu et al, 2018b ; Park et al, 2014 ; Petiwala et al, 2016 ; Kim et al, 2016 ).…”

Section: The Effectiveness Of Polyphenolsmentioning

confidence: 99%

“…Min et al (2021) GliomaIn vivo Cyclin B1, PARP, caspase-3, p-AKT, p62, LC3-I, and LC3-II Enhances TMZ-induced inhibition of colony formation and cell migration and enhances TMZ-induced cell cycle arrest and cellular apoptosis Shao et al , and AKT Suppresses the adhesion of tumor cells, as well as the secretion of MMP-9, TIMP-1, uPA, and VCAM-1, Mdm2, Bcl-2, and Bcl-xl, caspase-9, and -3, PARP, JAK2, Src kinases, STAT3, cyclin D1, D2, and D3 Induces apoptosis, inhibits the constitutive phosphorylation, inhibits cell viability and the expression of cyclin D1 and survivingKim et al (2016) …”

mentioning

confidence: 99%

Modern aspects of the use of natural polyphenols in tumor prevention and therapy

Суфианова

Gareev

Beylerli

et al. 2022

Front. Cell Dev. Biol.

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Polyphenols are secondary plant metabolites or organic compounds synthesized by them. In other words, these are molecules that are found in plants. Due to the wide variety of polyphenols and the plants in which they are found, these compounds are divided according to the source of origin, the function of the polyphenols, and their chemical structure; where the main ones are flavonoids. All the beneficial properties of polyphenols have not yet been studied, since this group of substances is very extensive and diverse. However, most polyphenols are known to be powerful antioxidants and have anti-inflammatory effects. Polyphenols help fight cell damage caused by free radicals and immune system components. In particular, polyphenols are credited with a preventive effect that helps protect the body from certain forms of cancer. The onset and progression of tumors may be related directly to oxidative stress, or inflammation. These processes can increase the amount of DNA damage and lead to loss of control over cell division. A number of studies have shown that oxidative stress uncontrolled by antioxidants or an uncontrolled and prolonged inflammatory process increases the risk of developing sarcoma, melanoma, and breast, lung, liver, and prostate cancer. Therefore, a more in-depth study of the effect of polyphenolic compounds on certain signaling pathways that determine the complex cascade of oncogenesis is a promising direction in the search for new methods for the prevention and treatment of tumors.

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“…Snail and Slug cooperate in EMT and tumor metastasis in oral tongue squamous cell carcinoma through MiR-101 mediated EZH2 axis ( 6 ). Carnosic acid inhibits the development of OSCC through mitochondrial mediated apoptosis ( 7 ). Commonly used diagnostic methods, such as serum tumor markers and imaging, are not ideal for OSCC and do not meet all clinical needs.…”

Section: Introductionmentioning

confidence: 99%

Bioinformatics based exploration of hsa-miR-194-5p regulation of CHD4 through PI3K/AKT signal pathway to enhance tumor resistance to apoptosis due to loss of nests and participate in poor prognosis of oral squamous cell carcinoma

Li¹,

Wang²,

Shen³

et al. 2023

Ann Transl Med

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Background Recent evidence shows that CHD4 is involved in a variety of biological events of tumors. Our aim was to investigate the correlation between CHD4 and oral squamous cell carcinoma (OSCC). Methods After CHD4 was screened as a differentially expressed gene in The Cancer Genome Atlas (TGCA) database, the correlations of its expression level with the clinical parameters and prognosis of patients with OSCC were analyzed. The outcomes of the multivariate analysis were used to construct a nomogram, and the accuracy of the model was evaluated with the calibration curve. The GeneMANIA and STRING databases were used to generate network diagrams depicting interactions of genes with CHD4, and heat maps of genes co-expressed with CHD4 were generated using the TCGA database. TargetScan was then used to look into the miRNAs that interact with the 3' untranslated region of CHD4 mRNA. Finally, GSEA enrichment analysis was used to explore the possible mechanism. Results The differentially expressed molecule CHD4 was screened by TCGA database for OSCC. CHD4 was overexpressed in OSCC tumor tissues, and OSCC patients with low expression of CHD4 have better OS and DSS. The nomogram had a C-index of 0.575 (0.548–0.602), which indicated some degree of predictive reliability. CHD4 has certain correlation with exons of OSCC related genes, including TP53 , NOTCH1 , CASP8 , PTEN , TP63 , ANXA1 , CDH1 , CTNNB1 , GDF15 and EGFR . According to the TargetScan database, hsa-miR-194-5p is the miRNA that regulates CHD4 upstream the most. GSEA analysis showed that CHD4 may participate in the poor prognosis of OSCC by participating in PI3K/AKT pathway, protein adhesion regulation, MAPK pathway, cytokine and inflammatory response regulation, angiogenesis and platelet regulation. Conclusions The decreased expression of CHD4 may indicate a better prognosis in OSCC patients and could serve as a novel predictive biomarker for OSCC. Also, hsa-miR-194-5p was found to contribute to the poor prognosis of OSCC by regulating CHD4 and enhancing tumor anoikis resistance via the PI3K/AKT signaling pathway. These findings suggest that CHD4 might be a therapeutic target for the effective treatment of OSCC.

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

Cited by 16 publications

References 54 publications

Lucialdehyde B suppresses proliferation and induces mitochondria-dependent apoptosis in nasopharyngeal carcinoma CNE2 cells

Lucialdehyde B suppresses proliferation and induces mitochondria-dependent apoptosis in nasopharyngeal carcinoma CNE2 cells

Modern aspects of the use of natural polyphenols in tumor prevention and therapy

Bioinformatics based exploration of hsa-miR-194-5p regulation of CHD4 through PI3K/AKT signal pathway to enhance tumor resistance to apoptosis due to loss of nests and participate in poor prognosis of oral squamous cell carcinoma

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