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S100A12 在甲状腺乳头状癌中是一种很有前途的生物标志物。

S100A12 is a promising biomarker in papillary thyroid cancer.

机构信息

Department of anatomy, Shenyang Medical College, Huanggu District, Shenyang City, Liaoning Province, 110034, P.R. China.

Department of Radiology, The Second Affiliated Hospital of Shenyang Medical College, Shenyang City, Liaoning Province, 110035, P.R. China.

出版信息

Sci Rep. 2020 Feb 3;10(1):1724. doi: 10.1038/s41598-020-58534-1.

DOI:10.1038/s41598-020-58534-1
PMID:32015423
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6997206/
Abstract

S100A12 belongs to the S100 family and acts as a vital regulator in different types of tumors. However, the function of S100A12 in thyroid carcinoma has not yet been investigated. In this study, we analyzed the expression of S100A12 in human papillary thyroid cancer (PTC) samples and two PTC cell lines. In addition, we explored the effects of S100A12 on PTC cell progression in vitro and in vivo. Our results showed that S100A12 was significantly upregulated in PTC specimens. Moreover, silencing S100A12 markedly inhibited PTC cell proliferation, migration, invasion and cell cycle progression. In addition, knockdown of S100A12 significantly reduced the expression of CyclinD1, CDK4 and p-ERK in PTC cells. An in vivo study also showed that silencing S100A12 dramatically suppressed tumor cell growth and decreased Ki67 expression in a xenograft mouse model. This study provides novel evidence that S100A12 serves as an oncogene in PTC. Knockdown of S100A12 suppressed PTC cell proliferation, migration, and invasion and induced G0/G1 phase arrest via the inhibition of the ERK signaling pathway. Therefore, S100A12 may be a potent therapeutic target for PTC.

摘要

S100A12 属于 S100 家族，在多种类型的肿瘤中充当重要的调节因子。然而，S100A12 在甲状腺癌中的功能尚未被研究。在本研究中，我们分析了 S100A12 在人甲状腺乳头状癌（PTC）样本和两种 PTC 细胞系中的表达。此外，我们还探讨了 S100A12 对 PTC 细胞在体外和体内进展的影响。我们的结果表明，S100A12 在 PTC 标本中显著上调。此外，沉默 S100A12 明显抑制 PTC 细胞增殖、迁移、侵袭和细胞周期进程。此外，S100A12 的敲低显著降低了 PTC 细胞中细胞周期蛋白 D1（CyclinD1）、细胞周期蛋白依赖性激酶 4（CDK4）和磷酸化 ERK（p-ERK）的表达。一项体内研究还表明，沉默 S100A12 可显著抑制肿瘤细胞生长，并降低异种移植小鼠模型中 Ki67 的表达。本研究提供了新的证据，表明 S100A12 作为 PTC 的致癌基因。S100A12 的敲低通过抑制 ERK 信号通路，抑制 PTC 细胞增殖、迁移和侵袭，并诱导 G0/G1 期阻滞。因此，S100A12 可能是 PTC 的一个有潜力的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/b9deab900799/41598_2020_58534_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/40dde8db8822/41598_2020_58534_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/113d16df1e3c/41598_2020_58534_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/8d180753c70d/41598_2020_58534_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/d5ea5c0c25d8/41598_2020_58534_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/b9deab900799/41598_2020_58534_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/40dde8db8822/41598_2020_58534_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/113d16df1e3c/41598_2020_58534_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/8d180753c70d/41598_2020_58534_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/d5ea5c0c25d8/41598_2020_58534_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ac/6997206/b9deab900799/41598_2020_58534_Fig5_HTML.jpg

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