基因敲除
竞争性内源性RNA
基因沉默
小RNA
癌症研究
生物
长非编码RNA
肺癌
分子生物学
细胞生物学
核糖核酸
基因
医学
生物化学
内科学
作者
Ninghuang Dai,Haitao Ma,Yu Feng
标识
DOI:10.14715/cmb/2023.69.9.29
摘要
Long non-coding RNAs (lncRNAs) play central roles in lung cancer progression by acting as competing endogenous RNAs (ceRNAs). This study aimed to explore the roles of lncRNA SDCBP2-AS1 in lung cancer and the molecular mechanism. The expression of SDCBP2-AS1, microRNA (miR)-656-3p, and cysteine-rich transmembrane BMP regulator 1 (CRIM1) was measured using quantitative real-time polymerase chain reaction. Ferroptosis was evaluated by analyzing cell death, ferrous content, reactive oxygen species (ROS) level, and protein levels of ferroptosis markers. The binding relationship was assessed using a dual-luciferase reporter assay. We observed that SDCBP2-AS1 was highly expressed in lung cancer cells. Knockdown of SDCBP2-AS1 promoted ferroptosis of lung cancer cells. SDCBP2-AS1 is a sponge of miR-656-3p, which directly targets CRIM1. Rescue experiments confirmed that SDCBP2-AS1 regulates ferroptosis by miR-656-3p, and overexpression of CRIM1 abrogated the effects of miR-656-3p on ferroptosis. In conclusion, depletion of SDCBP2-AS1 promoted lung cancer cell ferroptosis via the miR-656-3p/CRIM1 axis.
科研通智能强力驱动
Strongly Powered by AbleSci AI