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TFAP2A 通过 EMT 诱导 KRT16 作为肺腺癌的癌基因。

TFAP2A Induced KRT16 as an Oncogene in Lung Adenocarcinoma via EMT.

机构信息

Jiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address).

School Of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.

出版信息

Int J Biol Sci. 2019 Jun 2;15(7):1419-1428. doi: 10.7150/ijbs.34076. eCollection 2019.

DOI:10.7150/ijbs.34076
PMID:31337972
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6643144/
Abstract

: keratin 16 (KRT16) is a type I cytokeratin that overexpressed in many kinds of cancers, but unlike other keratins, KRT16 was poorly studied, so the aim of current study was to determine the biological role of KRT16 in lung adenocarcinoma (LUAD). : by utilizing open access data, we determined KRT16 expression in LUAD. After that we evaluated the biological role of KRT16 and . We also explored the reason for KRT16 overexpression. Last, we explored the clinical significance of KRT16 in LUAD. : we found KRT16 is overexpressed in LUAD and positively correlated with lymph node metastasis. Knockdown of KRT16 significantly influenced the LUAD cells' migration, invasion, proliferation and epithelial-mesenchymal transition (EMT). Moreover, TFAP2A could transcriptionally overexpress KRT16, which contributed to the TFAP2A tumorigenicity. Last, we determined that high level of KRT16 predicts poor prognosis of LUAD patients. : our data indicate that, TFAP2A induced KRT16 overexpression promotes tumorigenicity in LUAD via EMT, and KRT16 expression could serve as an independent prognosis marker.

摘要

角蛋白 16（KRT16）是一种 I 型细胞角蛋白，在许多癌症中过度表达，但与其他角蛋白不同，KRT16 的研究较少，因此目前的研究目的是确定 KRT16 在肺腺癌（LUAD）中的生物学作用。

通过利用公开数据，我们确定了 LUAD 中 KRT16 的表达。之后，我们评估了 KRT16 的生物学作用和机制。我们还探讨了 KRT16 过度表达的原因。最后，我们探讨了 KRT16 在 LUAD 中的临床意义。

我们发现 KRT16 在 LUAD 中过度表达，并与淋巴结转移呈正相关。敲低 KRT16 显著影响 LUAD 细胞的迁移、侵袭、增殖和上皮-间充质转化（EMT）。此外，TFAP2A 可以转录性地上调 KRT16 的表达，这有助于 TFAP2A 的致瘤性。最后，我们确定高水平的 KRT16 预示着 LUAD 患者预后不良。

我们的数据表明，TFAP2A 诱导的 KRT16 过度表达通过 EMT 促进 LUAD 的肿瘤发生，并且 KRT16 的表达可以作为独立的预后标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/4db629856533/ijbsv15p1419g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/13ef935c0546/ijbsv15p1419g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/d37e9236b58a/ijbsv15p1419g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/8fb423f808ab/ijbsv15p1419g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/8b5e870b82b2/ijbsv15p1419g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/4db629856533/ijbsv15p1419g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/13ef935c0546/ijbsv15p1419g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/d37e9236b58a/ijbsv15p1419g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/8fb423f808ab/ijbsv15p1419g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/8b5e870b82b2/ijbsv15p1419g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efa4/6643144/4db629856533/ijbsv15p1419g005.jpg

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