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Baicalein inhibits the growth of oral squamous cell carcinoma cells by downregulating the expression of transcription factor Sp1
Author(s) -
Zilong Gao,
Yaqian Zhang,
Heng Zhou,
Juan Lv
Publication year - 2019
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2019.4894
Subject(s) - baicalein , cell cycle , apoptosis , cancer research , cell growth , oncogene , gene knockdown , cell , biology , gene silencing , cell culture , western blot , chemistry , microbiology and biotechnology , pharmacology , biochemistry , genetics , gene
Oral squamous cell carcinoma (OSCC), the most common malignancy of the oral cavity, accounts for >90% of all diagnosed oral cancer cases. Baicalein, a naturally derived compound, has been shown to alter p65 and the nuclear factor (NF)‑κB pathway, thus exerting cytotoxic effects on various tumor cell types. However, the mechanism of action of baicalein in OSCC has not been fully elucidated. In the present study, the proliferation of OSCC cells treated with baicalein was examined using a CCK‑8 assay. The effects of baicalein on the cell cycle and apoptosis of OSCC cells were determined by flow cytometric analyses. The expression of specificity protein 1 (Sp1), p65 and p50 at the mRNA and protein levels was determined by reverse transcription‑quantitative PCR and western blot analysis, respectively. The results of the present study demonstrated that baicalein suppresses the proliferation of OSCC cell lines in vivo and in vitro. Baicalein also induced apoptosis of OSCC cells and arrested the cell cycle at the G0/G1 phase. Baicalein inhibited the expression of Sp1, p65 and p50 by downregulating the relative mRNA levels. Baicalein reduced the activity of NF‑κB in OSCC cells. Knockdown of Sp1 also resulted in reduced expression of p65 and p50. In addition, Sp1 silencing enhanced the effects of baicalein. In conclusion, the present study demonstrated that baicalein suppresses the growth of OSCC cells through an Sp1/NF‑κB‑dependent mechanism.

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