Plumbagin Enhances the Radiosensitivity of Tongue Squamous Cell Carcinoma Cells via Downregulating ATM

This study was designed to investigate whether plumbagin (PL) could sensitize ionizing radiation (IR) in tongue squamous cell carcinoma (TSCC) cells and its possible mechanisms. Cell proliferation and combination index analysis was based on MTT and colony formation assay. Flow cytometry was applied to analyze the cell cycle distribution and apoptosis after the treatment of PL and/or IR. RT-PCR was used to examine the gene expression level of ataxia telangiegatasiata muted (ATM) and nuclear factor kappa beta (NF- κB ) after various treatment groups. Western blot was used to examine the protein level of ATM and NF- κB as well as their phosphorylation level. PL enhances the cytotoxicity of IR in TSCC cells. Combination index was <1 which represents a synergistic effect. Combined PL and IR promoted G2/M arrest and apoptosis which could be reversed by ATM activator chloroquine phosphate. ATM and NF- κB were both inhibited by PL and IR combination. PL can efficiently enhance the radiosensitivity of TSCC cells by inducing G2/M arrest and apoptosis via downregulating ATM.

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Isoliquiritigenin Inhibits Proliferation and Induces Apoptosis in Tongue Squamous Cell Carcinoma by Modulating miR-21/FOXG1 Pathway

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.17:463-469 ◽

2019 ◽

Vol 17 (4) ◽

pp. 463-469

Author(s):

Hou Deqiang ◽

Gao Yufeng ◽

Bai Ning ◽

Dong Yu

Keyword(s):

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Carcinoma Cells ◽

Tongue Squamous Cell Carcinoma ◽

Luciferase Assay ◽

Forkhead Box ◽

Proliferation And Apoptosis ◽

Mrna And Protein Expression ◽

Induced Apoptosis

Isoliquiritigenin is a flavonoid commonly found in liquorice and has been identified as a potent anti-tumor agent. The aim of this study was to investigate whether isoliquiritigenin regulates the proliferation and apoptosis of tongue squamous cell carcinoma cells by regulating forkhead box G1 expression via miR-21. MTT assay and flow cytometry were used to analyze cell proliferation and apoptosis, respectively. Quantitative real time polymerase chain reaction and western blotting were used to detect mRNA and protein expression levels, respectively. The relationship between miR-21 and forkhead box G1 was detected by dual luciferase assay. Isoliquiritigenin inhibited proliferation and induced apoptosis of tongue squamous cell carcinoma cells, and decreased miR-21 levels and promoted forkhead box G1 expression. Forkhead box G1 was then identified as a target of miR-21 and ISL could promote forkhead box G1 expression by inhibiting miR-21. Further analysis suggested that upregulation of miR-21 improved proliferation and suppressed apoptosis of tongue squamous cell carcinoma cells by inhibiting forkhead box G1 expression. Finally, our results revealed that isoliquiritigenin inhibited proliferation and induced apoptosis of tongue squamous cell carcinoma cells by regulating miR-21. Isoliquiritigenin might act as a novel therapeutic treatment for tongue squamous cell carcinoma cells through up-regulation of forkhead box G1 expression via inhibiting miR-21expression.

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