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S100A6 通过 PI3K/AKT/mTOR 通路促进甲状腺癌的发展并抑制甲状腺癌细胞凋亡。

S100A6 promotes the development of thyroid cancer and inhibits apoptosis of thyroid cancer cells through the PI3K/AKT/mTOR pathway.

机构信息

Department of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR China.

Department of General Surgery, Breast and Thyroid Unit, Tribhuvan University Teaching Hospital, Kathmandu, Nepal.

出版信息

Pathol Res Pract. 2023 Feb;242:154325. doi: 10.1016/j.prp.2023.154325. Epub 2023 Jan 18.

Abstract

High levels of S100A6 have been associated with progression in some types of human cancers. Cancers related to S100A6 have been reported to include lung cancer, cervical cancer, pancreatic cancer, gastric cancer, colon cancer, etc., but its role in the molecular pathogenesis of these cancers is largely unknown. This study investigated the expression and functional roles of S100A6 in human thyroid cancer. The expression level of S100A6 in thyroid cancer cells was determined by bioinformatics and transcriptomic analysis. Furthermore, the potential functions of S100A6 in tumorigenesis were analyzed by cell proliferation, migration, invasion, and Western blot assays in human thyroid cancer cells. Public database queries revealed high S100A6 expression in thyroid cancer. In addition, we also found that high expression of S100A6 was positively correlated with malignant clinicopathological characteristics of thyroid cancer in The Cancer Genome Atlas database. qPCR results confirmed the high expression of S100A6 in thyroid cancer cells. S100A6 silencing inhibited cell proliferation, migration, and invasion. Western blot assays and response experiments showed that S100A6 promotes cell proliferation and tumorigenicity partly through the PI3K/AKT/mTOR signaling pathway. These results suggest that S100A6 affects the progression of thyroid cancer and can be used as a target in the future treatment of thyroid cancer.

摘要

高水平的 S100A6 与某些类型的人类癌症的进展有关。已经报道与 S100A6 相关的癌症包括肺癌、宫颈癌、胰腺癌、胃癌、结肠癌等,但它在这些癌症的分子发病机制中的作用在很大程度上是未知的。本研究调查了 S100A6 在人类甲状腺癌中的表达和功能作用。通过生物信息学和转录组分析确定甲状腺癌细胞中 S100A6 的表达水平。此外,通过细胞增殖、迁移、侵袭和 Western blot 分析在人甲状腺癌细胞中分析了 S100A6 在肿瘤发生中的潜在功能。公共数据库查询显示甲状腺癌中 S100A6 表达较高。此外,我们还发现,在 The Cancer Genome Atlas 数据库中,S100A6 的高表达与甲状腺癌恶性临床病理特征呈正相关。qPCR 结果证实了 S100A6 在甲状腺癌细胞中的高表达。S100A6 沉默抑制细胞增殖、迁移和侵袭。Western blot 分析和反应实验表明,S100A6 通过 PI3K/AKT/mTOR 信号通路促进细胞增殖和致瘤性。这些结果表明 S100A6 影响甲状腺癌的进展,可以作为未来甲状腺癌治疗的靶点。

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