Wang Xuguang, Fa Xian-En
Department of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450052 P. R. China.
Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Zhengzhou University No. 2 Jingba Road Zhengzhou 450014 P. R. China
RSC Adv. 2018 Mar 19;8(19):10610-10619. doi: 10.1039/c8ra00860d. eCollection 2018 Mar 13.
LncRNA urothelial carcinoma associated 1 (UCA1) was reported to be upregulated in non-small cell lung cancer (NSCLC) tissues and contributed to NSCLC progression. Additionally, it has been proposed that the oncogenic role of UCA1 may be related to glucose metabolism in bladder cancer. However, whether and how UCA1 regulates glucose metabolism in the progression of NSCLC remains unknown. Our results showed that knockdown of UCA1 inhibited the viability of NSCLC cells. UCA1 silencing suppressed glycolysis of NSCLC cells by reducing the glucose consumption and lactate production. Additionally, knockdown of UCA1 suppressed PKM2 expression and the mTOR pathway in NSCLC cells. Mechanistically, PKM2 knockdown suppressed the effects of UCA1 on viability and glycolysis of NSCLC cells and inhibition of the mTOR pathway suppressed the effects of UCA1 on viability, glycolysis, and PKM2 expression in NSCLC cells. In conclusion, knockdown of UCA1 inhibited viability and glycolysis by suppressing PKM2 expression maybe through the mTOR pathway in NSCLC cells, providing a novel insight into the molecular mechanism of UCA1 involved in the regulation of glucose metabolism in NSCLC cells.
据报道，长链非编码RNA尿路上皮癌相关1（UCA1）在非小细胞肺癌（NSCLC）组织中上调，并促进NSCLC进展。此外，有人提出UCA1的致癌作用可能与膀胱癌中的葡萄糖代谢有关。然而，UCA1在NSCLC进展过程中是否以及如何调节葡萄糖代谢仍不清楚。我们的结果表明，敲低UCA1可抑制NSCLC细胞的活力。UCA1沉默通过减少葡萄糖消耗和乳酸产生来抑制NSCLC细胞的糖酵解。此外，敲低UCA1可抑制NSCLC细胞中PKM2的表达和mTOR通路。机制上，PKM2敲低可抑制UCA1对NSCLC细胞活力和糖酵解的影响，而抑制mTOR通路可抑制UCA1对NSCLC细胞活力、糖酵解和PKM2表达的影响。总之，敲低UCA1可能通过mTOR通路抑制PKM2表达来抑制NSCLC细胞的活力和糖酵解，为UCA1参与调节NSCLC细胞葡萄糖代谢的分子机制提供了新的见解。
