Objective. The receptor-type tyrosine-protein phosphatase κ (PTPRK) is a candidate tumor suppressor involved in the tumorigenesis of various organs. However, its expression and biological roles in non-small-cell lung cancer (NSCLC) have not yet been investigated. Methods. PTPRK expression in NSCLC tissues and cell lines was examined using real-time PCR and western blotting. In addition, the effects of PTPRK on cell migration, invasion, and proliferation were evaluated in vitro. Furthermore, we explored whether the downregulation of PTPRK led to STAT3 activation in NSCLC cell lines by western blotting. The expression of phospho-STAT3^Tyr705 in primary human NSCLC tissues was evaluated by immunohistochemistry. Results. The results showed that PTPRK expression was frequently reduced in NSCLC tissues with lymph node metastasis and cell lines. The inhibition of PTPRK expression resulted in increased proliferation, invasion, and migration of NSCLC cells in vitro. Additionally, after silencing of PTPRK, phospho-STAT3^Tyr705 was significantly increased in NSCLC cells. Moreover, the phospho-STAT3^Tyr705 levels of NSCLC tissues were positively correlated with lymph node metastasis and significantly inversely correlated with the expression of PTPRK (). Conclusions. These results suggested that PTPRK functions as a novel tumor suppressor in NSCLC, and its suppressive ability may be involved in STAT3 activation.

中文翻译：

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PTPRK 下调通过增强 STAT3 激活促进 NSCLC 细胞增殖和转移。

客观。受体型酪氨酸蛋白磷酸酶κ (PTPRK) 是参与各种器官肿瘤发生的候选肿瘤抑制因子。然而，尚未研究其在非小细胞肺癌 (NSCLC) 中的表达和生物学作用。方法。使用实时 PCR 和蛋白质印迹检查 NSCLC 组织和细胞系中的 PTPRK 表达。此外，在体外评估了 PTPRK 对细胞迁移、侵袭和增殖的影响。此外，我们通过蛋白质印迹探讨了 PTPRK 的下调是否导致 NSCLC 细胞系中的 STAT3 激活。通过免疫组织化学评估原代人 NSCLC 组织中磷酸化 STAT3 ^{Tyr705的表达。}结果。结果表明，在有淋巴结转移的NSCLC组织和细胞系中，PTPRK的表达经常降低。PTPRK 表达的抑制导致 NSCLC 细胞在体外的增殖、侵袭和迁移增加。此外，在 PTPRK 沉默后，磷酸化 STAT3 ^Tyr705在 NSCLC 细胞中显着增加。此外，NSCLC组织的磷酸化STAT3 ^Tyr705水平与淋巴结转移呈正相关，与PTPRK的表达呈显着负相关。）。 结论。这些结果表明 PTPRK 在 NSCLC 中作为一种新型肿瘤抑制因子发挥作用，其抑制能力可能与 STAT3 激活有关。