Deoxyshikonin Mediates Heme Oxygenase-1 Induction and Apoptotic Response via p38 Signaling in Tongue Cancer Cell Lines

Deoxyshikonin (DSK), a phytochemical constituent, has been documented to elicit various oncostatic properties alone or in combination with established therapeutics. However, its role in restraining oral squamous cell carcinoma (OSCC) is mostly unclear. Here, we examined the tumor-suppressive effect...

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Published in:International journal of molecular sciences 2022-07, Vol.23 (13), p.7115
Main Authors: Chuang, Chun-Yi, Lin, Chiao-Wen, Su, Chun-Wen, Chen, Yi-Tzu, Yang, Wei-En, Yang, Shun-Fa, Su, Shih-Chi
Format: Article
Language:English
Subjects:
Apoptosis
Cancer therapies
Caspase-9
Cell cycle
Cell death
Cell viability
Chemotherapy
Colorectal cancer
deoxyshikonin
Disease
G1 phase
Heme
Heme oxygenase (decyclizing)
HO-1
Kinases
Leukemia
Lung cancer
Medical prognosis
Molecular modelling
Oral cancer
Oral carcinoma
Oral squamous cell carcinoma
OSCC
Oxygenase
p38
Phosphorylation
Phytochemicals
Proteins
Proteomes
Radiation therapy
Squamous cell carcinoma
Tongue
Tumor cell lines
Tumors
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Summary:Deoxyshikonin (DSK), a phytochemical constituent, has been documented to elicit various oncostatic properties alone or in combination with established therapeutics. However, its role in restraining oral squamous cell carcinoma (OSCC) is mostly unclear. Here, we examined the tumor-suppressive effect of DSK and explored the molecular mechanisms underlying DSK’s activities on controlling oral cancer. Our results showed that DSK dose-dependently lessened the cell viability of tongue cancer cell lines, involving induction of cell cycle arrest at the sub-G1 phase and apoptotic cell death. Moreover, a unique signature of apoptosis-related proteins, including augmented nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) expression and caspase activation, was observed in DSK-treated tongue cancer cell lines. Furthermore, DSK-mediated upregulation of HO-1 and cleavage of caspase-9 and -3 were significantly inhibited by pharmacological blockage of p38 kinase. Collectively, these data revealed that DSK halted cell cycle progression and elicited cell apoptosis in tongue cancer cell lines, reshaping a p38-dependent profile of apoptotic proteome. Our findings provided novel insights into the therapeutic implications of a natural compound on the management of OSCC.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms23137115