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. 2022 Feb 25;49(4):54. doi: 10.3892/ijmm.2022.5110

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Copyright: © Han et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Myricetin-induced autophagy is regulated by JNK in SK-BR-3 cell. (A) Cell viability (as measured by an MTT assay) of SK-BR-3 cells pretreated with SP600125 (a JNK inhibitor; 5 µM for 1 h) followed by treatment with myricetin (MYR) (10 µM for 24 h). (B) Western blot analysis of p-JNK, Bax, Bcl-2, and LC 3-II/I expression in SK-BR-3 cells. (C) Densitometric quantification of the bands in B. The control group (0 µM) was treated with the same amount of DMSO, and β-actin was used as a loading control. Data are displayed as the mean ± SD (n=3). ^*P<0.05 vs. control group; ^#P<0.05 vs. myricetin treatment group. MTT, 3-(4,5-dimethylthiazol-2-yl)-2.5-diphenyltetrazolium bromide; JNK, c-Jun N-terminal kinase; Bax, Bcl-2 associated X; Bcl-2, B cell lymphoma 2; LC 3, microtubule-associated protein 1A/1B-light chain 3; DMSO, dimethyl sulfoxide.