MYB Proto-Oncogene Like 2 (MYBL2) is a highly conserved member of the Myb family of transcription factors and plays a critical role in regulating cell proliferation and survival. Here we show that overexpression of MYBL2 is frequently observed in lung adenocarcinoma (LUAD) and significantly correlates with advanced stage and poor patient survival. Knockdown of MYBL2 induced apoptosis in lung cancer cells and resulted in significant inhibition of cell proliferation, migration, and invasion. Notably, we identified Non-SMC Condensin I Complex Subunit H (NCAPH) gene as a direct target of MYBL2. NCAPH expression is highly correlated with that of MYBL2 in LUAD cases and is tightly affected by MYBL2 knockdown or overexpression in vitro. Chromatin immunoprecipitation (ChIP) assays also showed that MYBL2 directly binds to the transcription start site (TSS) of NCAPH. Moreover, we provided evidence that NCAPH functions as an oncogene in lung cancer and overexpression of NCAPH could partially rescue cell death and migration blockage induced by MYBL2 knockdown. Together, these results suggest that overexpression of MYBL2 promotes proliferation and migration of lung cancer cells via upregulating NCAPH, establishing their roles as novel prognostic biomarkers as well as potential therapeutic targets for the disease.

中文翻译：

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MYBL2的过表达通过上调NCAPH促进非小细胞肺癌的增殖和迁移。

MYB原癌基因样2（MYBL2）是Myb转录因子家族的高度保守成员，在调节细胞增殖和存活中起关键作用。在这里，我们显示MYBL2的过表达在肺腺癌（LUAD）中经常被观察到，并且与晚期和患者生存差密切相关。敲低MYBL2诱导肺癌细胞凋亡，并显着抑制细胞增殖，迁移和侵袭。值得注意的是，我们确定非SMC凝缩素I复合物亚基H（NCAPH）基因为MYBL2的直接目标。在LUAD病例中，NCAPH表达与MYBL2高度相关，并在体外受到MYBL2敲低或过表达的紧密影响。染色质免疫沉淀（ChIP）分析还显示MYBL2直接与NCAPH的转录起始位点（TSS）结合。此外，我们提供的证据表明，NCAPH在肺癌中起癌基因的作用，而NCAPH的过表达可以部分挽救MYBL2敲低引起的细胞死亡和迁移阻滞。总之，这些结果表明，MYBL2的过表达通过上调NCAPH促进肺癌细胞的增殖和迁移，从而确立了它们作为新的预后生物标记物以及该疾病的潜在治疗靶标的作用。