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矢车菊素-3-O-葡萄糖苷通过上调 miR-214-5p 抑制 β-连环蛋白/MGMT 通路，逆转胶质瘤细胞的化疗耐药性。

Cyanidin-3-O-glucoside inhibits the β-catenin/MGMT pathway by upregulating miR-214-5p to reverse chemotherapy resistance in glioma cells.

机构信息

College of Pharmacy, Hubei University of Chinese Medicine, No. 16 Huangjiahu West Road, Huangjiahu University Town, Hongshan District, Wuhan, 430065, Hubei, China.

Department of Pharmacy, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.

出版信息

Sci Rep. 2022 May 11;12(1):7773. doi: 10.1038/s41598-022-11757-w.

DOI:10.1038/s41598-022-11757-w
PMID:35545654
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9095653/
Abstract

Overcoming resistance to alkylating agents has important clinical significance in glioma. Cyanidin-3-O-glucoside (C3G) has a tumor-suppressive effect on tumor cells. However, whether it plays a role in temozolomide resistance in glioma is still unclear. We constructed a TMZ-resistant LN-18/TR glioma cell line, observed the effect of C3G on TMZ resistance in this cell line, and explored the role of miR-214-5p in chemoresistance. Results showed that β-catenin and MGMT were significantly upregulated in LN-18/TR cells. C3G upregulated miR-214-5p and enhanced the cytotoxic effect of temozolomide on LN-18/TR cells. Contrarily, C3G downregulated β-catenin and MGMT. Moreover, the miR-214-5p mimic downregulated β-catenin and MGMT in LN-18/TR cells, whereas the miR-214-5p inhibitor had the opposite effect; the miR-214-5p inhibitor significantly blocked the C3G-induced downregulation of β-catenin and MGMT. C3G or the miR-214-5p mimic enhanced temozolomide-induced apoptosis in LN-18/TR cells, whereas the miR-214-5p inhibitor blocked this effect. Furthermore, C3G or miR-214-5p agomir combined with TMZ significantly inhibited the growth of LN-18/TR tumors. Collectively, our research discovered the potential signaling mechanism associated with C3G-mediated suppression of TMZ resistance in LN-18/TR cells through miR-214-5p, which can facilitate the treatment of MGMT-induced resistance in glioma cells.

摘要

克服烷基化剂耐药性在神经胶质瘤中具有重要的临床意义。矢车菊素-3-O-葡萄糖苷（C3G）对肿瘤细胞具有肿瘤抑制作用。然而，它是否在神经胶质瘤替莫唑胺耐药中起作用尚不清楚。我们构建了 TMZ 耐药 LN-18/TR 神经胶质瘤细胞系，观察了 C3G 对该细胞系 TMZ 耐药的影响，并探讨了 miR-214-5p 在化疗耐药中的作用。结果表明，β-连环蛋白和 MGMT 在 LN-18/TR 细胞中显著上调。C3G 上调了 miR-214-5p，增强了替莫唑胺对 LN-18/TR 细胞的细胞毒性作用。相反，C3G 下调了β-连环蛋白和 MGMT。此外，miR-214-5p 模拟物下调了 LN-18/TR 细胞中的β-连环蛋白和 MGMT，而 miR-214-5p 抑制剂则产生相反的效果；miR-214-5p 抑制剂显著阻断了 C3G 诱导的β-连环蛋白和 MGMT 的下调。C3G 或 miR-214-5p 模拟物增强了 LN-18/TR 细胞中替莫唑胺诱导的细胞凋亡，而 miR-214-5p 抑制剂阻断了这种作用。此外，C3G 或 miR-214-5p 激动剂与 TMZ 联合显著抑制了 LN-18/TR 肿瘤的生长。总之，我们的研究发现了与 C3G 介导的 LN-18/TR 细胞 TMZ 耐药性抑制相关的潜在信号机制，这可能有助于治疗神经胶质瘤细胞中 MGMT 诱导的耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af4/9095653/a8f3fb14bde1/41598_2022_11757_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af4/9095653/a8f3fb14bde1/41598_2022_11757_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af4/9095653/ca70ab87c39d/41598_2022_11757_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af4/9095653/3473e2ff9f80/41598_2022_11757_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af4/9095653/23b5c4315028/41598_2022_11757_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af4/9095653/60238c788a87/41598_2022_11757_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af4/9095653/e02cc8d4439b/41598_2022_11757_Fig7_HTML.jpg
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