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Abstract Title:

Shikonin induces tumor apoptosis in glioma cells via endoplasmic reticulum stress, and Bax/Bak mediated mitochondrial outer membrane permeability.

Abstract Source:

J Ethnopharmacol. 2020 Jul 11:113059. Epub 2020 Jul 11. PMID: 32663591

Abstract Author(s):

Xiaoqin Ma, Meixiang Yu, Chenxia Hao, Wanhua Yang

Article Affiliation:

Xiaoqin Ma

Abstract:

ETHNOPHARMACOLOGICAL RELEVANCE: Shikonin, one of the main active ingredients of Chinese herbal medicine Lithospermum erythrorhizon, has been widely used to treat various disease including virus infection and inflammation in clinical. Its anti-tumor activity has been recorded in"Chinese herbal medicine". Recently, some studies about its anti-glioma effects have been reported. However, little is known about the molecular pharmacological activity of Shikonin in glioma.

AIM: This study aimed to systematically uncover and validate the pharmacological mechanism of Shikonin against glioma.

MATERIAL AND METHODS: Network pharmacology approach, survival analysis, and Pearson co-expression analysis were performed to uncover and test the pharmacological mechanisms of Shikonin in glioma. Apoptosis assay, Caspase-3 activity assay and immunoblot analysis were practiced to validate the mechanisms.

RESULTS: Network pharmacology results suggested, anti-glioma effect of Shikonin by interfering endoplasmic reticulum (ER) stress-mediated tumor apoptosis targeting Caspase-3, and Bax/Bak-induced mitochondrial outer membrane permeabilization (MOMP) triggering cancer cell apoptosis. Survival analysis suggested the association of CASP3 with glioma (P < 0.05). Pearson correlation analysis indicated possible interaction of CASP3 with PERK through positive feedback regulation. Shikonin or in combination with 14G2a induced cell apoptosis in oligodendroglioma Hs683 cells in a dose-dependent manner with at a maximum apoptosis rate of 33%-37.5%, and73%-77% respectively. Immunoblot analysis showed that Shikonin increased Caspase-3 activity to about 4.29 times, and increased 9 times when it combined with 14G2a. Shikonin increased also the expression levels of the proteins PERK and CHOP by about 4.4 and 5.6 folds, respectively, when it combinedwith 14G2a.

CONCLUSIONS: This study highlights the pharmacological mechanisms of Shikonin in the induction of tumor apoptosis in glioma cells.

Study Type : In Vitro Study
Additional Links
Pharmacological Actions : Apoptotic : CK(5217) : AC(3846)

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