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寇塔酮通过活性氧和蛋白激酶 B 通路诱导口腔癌细胞凋亡。

Costunolide Induces Apoptosis via the Reactive Oxygen Species and Protein Kinase B Pathway in Oral Cancer Cells.

机构信息

Department of Animal Science and Biotechnology, ITRD, Kyungpook National University, Sangju 37224, Korea.

Gyeongbuk Livestock Research Institute, Yeongju 36052, Korea.

出版信息

Int J Mol Sci. 2021 Jul 13;22(14):7509. doi: 10.3390/ijms22147509.

DOI:10.3390/ijms22147509
PMID:34299129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8305390/
Abstract

Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain unclear. This study investigated the potential anticancer ability and underlying mechanisms of CTD in OC in vivo and in vitro. Cell viability and anchorage-independent colony formation assays were performed to examine the antigrowth effects of CTD on OC cells; assessments for migration and invasion of OC cells were conducted by transwell; Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. The results revealed that CTD suppressed the proliferation, migration and invasion of oral cancer cells effectively and induced cell cycle arrest and apoptosis; regarding the mechanism, CTD bound to AKT directly by binding assay and repressed AKT activities through kinase assay, which thereby downregulating the downstream of AKT. Furthermore, CTD remarkably promotes the generation of reactive oxygen species by flow cytometry assay, leading to cell apoptosis. Notably, CTD strongly suppresses cell-derived xenograft OC tumor growth in an in vivo mouse model. In conclusion, our results suggested that costunolide might prevent progression of OC and promise to be a novel AKT inhibitor.

摘要

口腔癌 (OC) 近年来因其高发病率和死亡率而引起了研究关注。寇塔烯 (CTD) 具有多种癌症的潜在抗癌和生物活性能力已得到证实。然而，其对口腔癌的影响尚不清楚。本研究在体内和体外研究了 CTD 对 OC 的潜在抗癌能力和作用机制。通过细胞活力和非锚定依赖性集落形成测定来检查 CTD 对 OC 细胞的生长抑制作用；通过 Transwell 评估 OC 细胞的迁移和侵袭；通过流式细胞术研究细胞周期和凋亡，并通过免疫印迹进行验证。结果表明，CTD 有效抑制口腔癌细胞的增殖、迁移和侵袭，并诱导细胞周期停滞和凋亡；关于机制，通过结合测定，CTD 直接与 AKT 结合，并通过激酶测定抑制 AKT 活性，从而下调 AKT 的下游。此外，通过流式细胞术测定，CTD 显著促进活性氧的产生，导致细胞凋亡。值得注意的是，CTD 在体内小鼠模型中强烈抑制细胞源性异种移植物 OC 肿瘤的生长。总之，我们的结果表明寇塔烯可能预防 OC 的进展，并有望成为一种新型 AKT 抑制剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6066/8305390/59957d75387a/ijms-22-07509-g010.jpg
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