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首页> 外文期刊>RSC Advances >Knockdown of UCA1 inhibits viability and glycolysis by suppressing PKM2 expression through the mTOR pathway in non-small cell lung cancer cells
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Knockdown of UCA1 inhibits viability and glycolysis by suppressing PKM2 expression through the mTOR pathway in non-small cell lung cancer cells

机译：在非小细胞肺癌细胞中，敲低UCA1可以通过mTOR途径抑制PKM2表达，从而抑制活力和糖酵解

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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.
机译：据报道，LncRNA尿路上皮癌相关蛋白1（UCA1）在非小细胞肺癌（NSCLC）组织中表达上调，并有助于NSCLC的进展。另外，已经提出UCA1的致癌作用可能与膀胱癌中的葡萄糖代谢有关。但是，UCA1是否以及如何在非小细胞肺癌的发展过程中调节葡萄糖的代谢仍然未知。我们的结果表明，敲低UCA1抑制了NSCLC细胞的活力。 UCA1沉默通过减少葡萄糖消耗和乳酸生成来抑制NSCLC细胞的糖酵解。此外，敲除UCA1可抑制NSCLC细胞中PKM2的表达和mTOR途径。从机制上讲，PKM2敲低抑制了UCA1对NSCLC细胞的活力和糖酵解的影响，而抑制mTOR途径抑制了UCA1对NSCLC细胞的生存力，糖酵解和PKM2表达的影响。总之，敲低UCA1可能通过抑制NSKC细胞中的mTOR通路来抑制PKM2表达，从而抑制了细胞的活力和糖酵解，从而为UCA1参与调控NSCLC细胞葡萄糖代谢的分子机制提供了新的见识。

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