Wogonin induces cellular senescence in breast cancer via suppressing TXNRD2 expression.

Archives of Toxicology
Dawei YangNa Lu

Abstract

Cellular senescence contributes to tumor regression through both cell autonomous and non-autonomous mechanisms. Drugs inducing cancer cell senescence and modulating senescence-associated secretory phenotype (SASP) render advantage to the cancer treatment. Breast cancer remains the second most cause of female cancer mortality, among which triple-negative breast cancer (TNBC) has a more aggressive clinical course. Our study showed that in TNBC cell lines including MDA-MB-231 and 4T1 cells, moderate concentrations of wogonin (5, 7-dihydroxy-8-methoxy-2-phenyl-4h-1-benzopyran-4-one) (50-100 μM) not only induced permanent proliferation inhibition, but also increased P16 expression, β-galactosidase activity, senescence-associated heterochromatin foci and SASP, which are the typical characteristics of cellular senescence. Moreover, results showed that wogonin-induced senescence was partially attributed to the reactive oxygen species (ROS) accumulation upon wogonin treatment in MDA-MB-231 cells, since elimination of ROS by N-acetylcysteine (NAC) was able to repress wogonin-induced β-galactosidase activity. Mechanistically, wogonin reduced the expression of TXNRD2, an important antioxidant enzyme in controlling the levels of cellular RO...Continue Reading

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Citations

Apr 23, 2021·The International Journal of Biological Markers·Erika KorobeinikovaElona Juozaityte
Jul 3, 2021·International Journal of Molecular Sciences·Anna Domaszewska-SzostekAlina Kuryłowicz

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Methods Mentioned

BETA
ELISA
PMA
flow cytometry
immunoprecipitation
PCR
acetylation
histone acetylation
xenografts

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