Twist相关蛋白2(TWIST2)在骨发育中发挥重要作用,肿瘤发生,肿瘤进展和上皮间质转化(EMT)。目前,关于TWIST2在肺癌中的作用的报道很少,这需要进一步探索。因此,本研究旨在探讨TWIST2在肺癌发生发展中的作用及分子机制。使用RT-qPCR和蛋白质印迹法测量患者组织和细胞系中TWIST2的表达。MTT和CCK8测定用于检测细胞增殖和活力。蛋白质印迹法检测EMT相关蛋白的表达,包括E-cadherin,N-钙黏着蛋白,波形蛋白和鼻塞。结果表明,TWIST2在肺癌患者和细胞系的组织中表达较低。进一步研究发现,TWIST2过表达显著诱导细胞凋亡,促进E-cadherin的表达,以及抑制N-钙粘蛋白的表达,波形蛋白和鼻塞。更重要的是,TWIST2在肺癌细胞中诱导氧化应激。此外,TWIST2调节FGF21和AMPK/mTOR信号通路,这与肺癌细胞中基因的分子机制有关。我们认为TWIST2抑制肺癌进展的机制是通过调节FGF21介导的AMPK/mTOR信号通路。
Twist related protein 2 (
TWIST2) plays an important role in bone development, tumorigenesis, tumour progression and epithelial mesenchymal transition (EMT). At present, there are few reports about the role of TWIST2 in lung cancer, which need to be further explored. Therefore, the purpose of this study is to explore the role and molecular mechanism of
TWIST2 in the occurrence and development of lung cancer. The expression of
TWIST2 in tissues of patients and cell lines was measured using RT-qPCR and western blotting. MTT and CCK8 assays were used to detect cell proliferation and viability. Western blotting was used to measure the expression of EMT-related proteins, including E-cadherin, N-cadherin, Vimentin and Slug. The results revealed that TWIST2 is lowly expressed in the tissues of lung cancer patients and cell lines. Further studies found that overexpression of
TWIST2 significantly induced apoptosis and promoted the expression of E-cadherin, as well as inhibiting the expression of N-cadherin, Vimentin and Slug. More importantly,
TWIST2 induced oxidative stress in lung cancer cells. In addition, TWIST2 regulated the FGF21 and AMPK/mTOR signalling pathway, which is involved in the molecular mechanism of the gene in lung cancer cells. We suggest that the mechanism of TWIST2 inhibition of the progression of lung cancer is by regulating the FGF21-mediated AMPK/mTOR signalling pathway.