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Abstract：
Objectives: 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). Materials and Methods: by utilizing open access data, we determined KRT16 expression in LUAD. After that we evaluated the biological role of KRT16 in-vitro and in-vivo. We also explored the reason for KRT16 overexpression. Last, we explored the clinical significance of KRT16 in LUAD. Results: 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. Conclusions: 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：
目的:角蛋白16(KRT16)是一种I型细胞角蛋白,在多种肿瘤中过度表达,但与其他角蛋白不同,KRT16的研究很少，因此，本研究的目的是确定KRT16在肺腺癌（LUAD）中的生物学作用。材料和方法：通过利用开放访问数据，我们确定了LUAD中KRT16的表达。之后，我们在体外和体内评估了KRT16的生物学作用。我们还探讨了KRT16过表达的原因。最后,我们探讨了KRT16在LUAD中的临床意义。结果：我们发现KRT16在LUAD中过表达，并且与淋巴结转移呈正相关。敲除KRT16显著影响LUAD细胞的迁移，入侵,增殖和上皮间质转化（EMT）。此外，TFAP2A可以转录过表达KRT16，这有助于TFAP2A的致瘤性。最后,我们确定高水平的KRT16预测LUAD患者的预后不良.结论：我们的数据表明，TFAP2A诱导的KRT16过表达通过EMT促进LUAD的致瘤性，KRT16表达可作为独立的预后标志物。
