BACKGROUND Lung adenocarcinoma (LUAD) is a more frequent subtype of lung cancer and most cases are discovered in the late stages. The proliferation and metastasis of LUAD are pivotal for disease progression. Despite unremitting deeper understanding of LUAD biology, the mechanisms involved in the proliferation and metastasis of LUAD remain unclear. The objective of our article was to inquiry the expression and the function of keratin 6C (KRT6C) in LUAD cells. METHODS First, the expression level and prognostic value of KRT6C in LUAD tissues were analyzed on the basis of the data acquired from TCGA database. Through qRT-PCR, the expression level of KRT6C on LUAD cell lines (A549, H1299, PC-9) and human normal lung cell line MRC-5 was tested. After that, CCK8 and colony formation assays was utilized to detect cell proliferation. In addition, to explore the influence of KRT6C on LUAD migration and invasion ability, scratch wound healing and transwell assays were utilized. Through western blotting, the protein expression levels of KRT6C, PCNA, E-cadherin, N-cadherin, Snail and Vimentin were detected. RESULTS The outcomes revealed that KRT6C was highly expressed in LUAD tissues and cell lines. Besides, elevated level of KRT6C was related to worse prognosis in LUAD patients. Ablation of KRT6C restrained proliferation, migration and invasion of A549 cells. KRT6C deficiency augmented the expression of E-cadherin as well as reduced the expression of N-cadherin, Snail and Vimentin. CONCLUSION Above all, these consequences indicated that depletion of KRT6C suppressed A549 cell proliferation, migration and invasion, which might be achieved by regulating EMT. In general, KRT6C is identified as a potential therapeutic target for LUAD.

中文翻译：

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角蛋白6C的高表达与不良预后有关，并通过调节肺腺癌的上皮-间质转化来加速癌症的增殖和迁移。

背景技术肺腺癌（LUAD）是一种更常见的肺癌亚型，大多数病例是在晚期发现的。LUAD的增殖和转移对于疾病进展至关重要。尽管对LUAD生物学有不懈的深入了解，但参与LUAD增殖和转移的机制仍不清楚。本文的目的是研究LUAD细胞中角蛋白6C（KRT6C）的表达和功能。方法首先，根据从TCGA数据库获得的数据，分析KRT6C在LUAD组织中的表达水平和预后价值。通过qRT-PCR，测试了KRT6C在LUAD细胞系（A549，H1299，PC-9）和人正常肺细胞系MRC-5上的表达水平。之后，利用CCK8和集落形成测定法检测细胞增殖。此外，为了探索KRT6C对LUAD迁移和侵袭能力的影响，使用了刮擦伤口愈合和transwell分析法。通过蛋白质印迹法检测了KRT6C，PCNA，E-cadherin，N-cadherin，Snail和Vimentin的蛋白表达水平。结果结果表明，KRT6C在LUAD组织和细胞系中高表达。此外，LUAD患者KRT6C水平升高与预后不良有关。KRT6C的消融抑制了A549细胞的增殖，迁移和侵袭。KRT6C缺乏增加了E-钙粘蛋白的表达，并减少了N-钙粘蛋白，Snail和波形蛋白的表达。结论最重要的是，这些后果表明，KRT6C的耗竭抑制了A549细胞的增殖，迁移和侵袭，这可以通过调节EMT来实现。一般来说，