Tanshinone IIA effects on ovarian cancer cell line

Li, Nan; Yang, Liang; Zhang, Baolian; Yang, Keqin

doi:10.1111/jphp.12961

Cited by 24 publications

(17 citation statements)

References 27 publications

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“…Former work suggests that Tan promotes cell apoptosis by regulating inverted formin 2‐related mitochondrial fission and mammalian STE20‐like kinase 1‐Hippo pathway in colorectal cancer . In addition, Tan contributes to cell apoptosis and inhibits cell proliferation by upregulating miR‐205 in ovarian cancer . Besides, Tan has been indicated as a cardioprotective compound during atherosclerosis, thrombosis, and myocardial infarction reperfusion .…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA inhibits the adipogenesis and inflammatory response in ox‐LDL‐challenged human monocyte‐derived macrophages via regulating miR‐130b/WNT5A

Limei

Zhang

Liu

et al. 2019

J of Cellular Biochemistry

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Atherosclerosis is a kind of chronic cardiovascular disease, characterized by oxidized low‐density lipoprotein (ox‐LDL) accumulation in macrophage. Tanshinone IIA (Tan), a lipophilic pharmacologically activate compound from Salvia miltiorrhiza Bunge, has been indicated to exert cardioprotective roles. Nevertheless, the biological role of Tan and regulatory mechanism in atherosclerosis are not fully established. In present study, atherosclerosis model was established in THP‐1‐derived macrophages by treatment of ox‐LDL. The adipogenesis was measured by Nile red staining. The expressions of inflammatory factors, microRNA‐130b (miR‐130b) and WNT5A were measured by quantitative real‐time polymerase chain reaction or Western blot. The target association between miR‐130b and WNT5A was explored via luciferase activity and RNA immunoprecipitation assay. The results showed that exposure of Tan inhibited ox‐LDL‐induced adipogenesis and expressions of interleukin‐1β (IL‐1β), IL‐6, and tumor necrosis factor‐alpha in THP‐1‐derived macrophages. miR‐130b expression was decreased in THP‐1‐derived macrophages treated by ox‐LDL and its overexpression attenuated adipogenesis as well as inflammatory response. miR‐130b knockdown reversed the regulatory effect of Tan on adipogenesis and inflammatory response in THP‐1‐derived macrophages stimulated by ox‐LDL. In addition, WNT5A acted as a functional target of miR‐130b and inhibited by Tan and miR‐130b. As a conclusion, Tan decreased the adipogenesis and inflammatory response by mediating miR‐130b and WNT5A, providing a novel theoretical foundation for treatment of atherosclerosis.

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Section: Introductionmentioning

confidence: 99%

Tanshinone IIA inhibits the adipogenesis and inflammatory response in ox‐LDL‐challenged human monocyte‐derived macrophages via regulating miR‐130b/WNT5A

Limei

Zhang

Liu

et al. 2019

J of Cellular Biochemistry

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“…Tan IIA, which is derived from Salvia miltiorrhiza, has been proved to have antioxidant, coronary artery dilatation and anti-in ammatory effects [15][16]. Recent studies have shown that Tan IIA has anti-cancer effect in many malignant tumors, such as colon cancer, breast cancer, ovarian cancer [17][18][19]. Our previous studies demonstrated that Tan IIA had an effect on the invasion and metastasis of CRC [9].…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA Inhibits Epithelial-to-mesenchymal Transition Through Regulating β-arrestin1 Mediated β-catenin Signaling Pathway in Colorectal Cancer

Song

Yang

Han

et al. 2020

Preprint

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Background: Tanshinone IIA (Tan IIA) is a major active ingredient extracted from Salvia miltiorrhiza, which has been proved to inhibit metastasis of various cancers including colorectal cancer (CRC). However, the detailed mechanisms of Tan IIA against CRC metastasis are not well explored. Epithelial-to-mesenchymal transition (EMT) exerts an important regulatory role in CRC metastasis, and our previous mechanism studies demonstrated that β-arrestin1 could regulate CRC EMT partly through β-catenin signaling pathway. Therefore, in this work we investigated whether Tan IIA could regulate CRC EMT through β-arrestin1-mediated β-catenin signaling pathway in vivo and in vitro.Methods: The nude mice tail vein metastasis model was established to observe the effect of Tan IIA on CRC lung metastasis in vivo. The lung metastasis was evaluated by living animal imaging and hemaoxylin-eosin staining. The migratory ability of CRC cells in vitro were measured by transwell and wound healing assays. The protein expression and cellular localization of β-arrestin1 and β-catenin were characterized by immunofluorescence staining and western blot. The β-catenin signaling pathway related proteins and EMT associated proteins in CRC cells were detected by western blot and immunohistochemistry. Results: Our results showed that Tan IIA inhibited the lung metastases of CRC cells in vivo and extended the survival time of nude mice. In vitro, Tan IIA increased the expression of E-cadherin, decreased the secretion of Snail, N-cadherin and Vimentin, thus suppressed EMT and the migratory ability of CRC cells. Further study found the mechanism involving in Tan IIA regulating EMT and metastasis, referring to the suppression of β-arrestin1 expression, reduction of β-catenin nuclear localization, thereby the decreased activity of β-catenin signaling. Conclusion: Our data revealed a new mechanism of Tan IIA on the suppression of EMT and metastasis in CRC via β-arrestin1-mediated β-catenin signaling pathway, and provided support for Tan IIA as anti-metastatic agents in CRC.

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“…Coincidentally, T2A induced hepatocellular carcinoma (HCC) cell death by inducing apoptosis and cell cycle arrest, when T2A treat HCC cells, miR‐30b was down‐regulated which was the upstream of tumor protein 53 (TP53), that is to say the underlying mechanism involved in T2A induced cell death may be miR‐30b‐p53 pathway (Ren et al, 2017). Meanwhile, miR‐205 was predicted as the regulatory microRNA on surviving expression, recently studies showed that T2A also induced cell apoptosis by direct upregulation of miR‐205 in ovarian carcinoma (OC) TOV‐21G cells (N. Li, Yang, Zhang, & Chen, 2018).…”

Section: Tanshinones and Mirnasmentioning

confidence: 99%

Roles of plant‐derived bioactive compounds and relatedmicroRNAsin cancer therapy

Zou

Liu

et al. 2020

Phytotherapy Research

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Plant-derived bioactive compounds, often called phytochemicals, are active substances extracted from different plants. These bioactive compounds can release therapeutic potential abilities via reducing antitumor drugs side effects or directly killing cancer cells, and others also can adjust cancer initiation and progression via regulating microRNAs (miRNAs) expression, and miRNA can regulate protein-coding expression by restraining translation or degrading target mRNA. A mass of research showed that plant-derived bioactive compounds including tanshinones, astragaloside IV, berberine, ginsenosides and matrine can inhibit tumor growth and metastasis by rescuing aberrant miRNAs expression, which has influence on tumor progression, microenvironment and drug resistance in multifarious cancers. This review aims to provide a novel understanding of plant-derived bioactive compounds targeting miRNAs and shed light on their future clinical applications.

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Tanshinone IIA effects on ovarian cancer cell line

Abstract: Our data suggested that Tanshinone IIA induced cell apoptosis in ovarian carcinoma TOV-21G cells via direct upregulation of miR-205. Our study highlighted the potential therapeutic application of Tanshinone IIA against ovarian malignancy.

Cited by 24 publications

References 27 publications

Tanshinone IIA inhibits the adipogenesis and inflammatory response in ox‐LDL‐challenged human monocyte‐derived macrophages via regulating miR‐130b/WNT5A

Tanshinone IIA inhibits the adipogenesis and inflammatory response in ox‐LDL‐challenged human monocyte‐derived macrophages via regulating miR‐130b/WNT5A

Tanshinone IIA Inhibits Epithelial-to-mesenchymal Transition Through Regulating β-arrestin1 Mediated β-catenin Signaling Pathway in Colorectal Cancer

Roles of plant‐derived bioactive compounds and relatedmicroRNAsin cancer therapy

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