Human Schlafen 5 Inhibits Proliferation and Promotes Apoptosis in Lung Adenocarcinoma via the PTEN/PI3K/AKT/mTOR Pathway.
Xuefeng GuLi ZhouLei ChenHuiqing PanRui ZhaoWeiwei GuangGuoqing WanPeng ZhangDingsheng LiuLi-Li DengWeiming ZhaoChanglian LuPublished in: BioMed research international (2021)
We found that knockdown of endogenous SLFN5 upregulates cancer cell proliferation while inhibiting apoptosis. Besides, SLFN5 inhibition on proliferation was also observed in a nude mouse xenograft model. In contrast, overexpression of exogenous SLFN5 inhibited cell proliferation in vitro and in vivo and promoted apoptosis. As to the signaling pathway, we found phosphatase and tensin homolog on chromosome 10 (PTEN) was positively regulated by SLFN5, while its downstream signaling pathway AKT/mammalian target of rapamycin (mTOR) was inhibited. Moreover, compared with adjacent normal tissues, SLFN5 protein levels were markedly decreased in lung adenocarcinoma tissues. In conclusion, these suggest that human SLFN5 plays inhibitory roles in LUAC progression through the PTEN/PI3K/AKT/mTOR pathway, providing a potential target for developing drugs for lung cancer therapy in the future.
Keyphrases
- pi k akt
- cell proliferation
- cell cycle arrest
- signaling pathway
- endothelial cells
- cell cycle
- endoplasmic reticulum stress
- oxidative stress
- cancer therapy
- induced apoptosis
- epithelial mesenchymal transition
- gene expression
- induced pluripotent stem cells
- cell death
- magnetic resonance
- drug delivery
- squamous cell carcinoma
- papillary thyroid
- pluripotent stem cells
- magnetic resonance imaging
- binding protein
- dna methylation
- amino acid
- contrast enhanced
- drug induced
- risk assessment
- computed tomography
- protein kinase
- lymph node metastasis
- genome wide
- human health