Sevoflurane Inhibits lncRNA HOTAIR-Modulated Stability of HK2 mRNA in a m6A-Dependent Manner to Dampen Aerobic Glycolysis and Proliferation in Lung Cancer

七氟烷通过m6A依赖的方式抑制lncRNA HOTAIR调控的HK2 mRNA稳定性,从而抑制肺癌细胞的有氧糖酵解和增殖。

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Abstract

Previous studies have shown that sevoflurane has an inhibitory effect on tumor cells. So far, the effect of sevoflurane on hepatocellular carcinoma needs to be confirmed by more studies. HOX transcript antisense intergenic RNA (HOTAIR), a long noncoding RNA (lncRNA), has been shown to enhance cancer cell proliferation and medication resistance. The inherent importance and biological function of HOTAIR in the course of lung cancer (LC) is, however, poorly unclear. HOTAIR was shown to be highly elevated in LC cells in this investigation. Impairment of function trials with sevoflurane indicated that it has anticancer effects on LC cell growth, apoptosis, and aerobic glycolysis. In a mechanistic manner, HOTAIR was related to HK2 mRNA and promoted expression and constancy. Additional research revealed that HOTAIR coupled with hexokinase 2 (HK2) mRNA and favorably controlled its stabilization in a traditional-component way. By HK2, the LC enhancement role was mediated. In summary, our data show that HOTAIR promotes the synthesis and proliferation of LC glycogen by increasing the transcription of HK2, and HOTAIR is likely to be a potential treatment for LC patients.

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