Differential effects of nesfatin-1 on proliferation and migration in normal and cancerous human lung cells via the PI3K/AKT pathway.

Nesfatin-1, initially identified as an appetite-regulating hormone, has also been detected in various cancer tissues and implicated in tumorigenesis. However, its role in the proliferation and migration of lung cancer cells remains unclear. This study aims to investigate the effects of nesfatin-1 on the proliferation and migration of human lung cancer cells and elucidate the underlying molecular mechanisms. The expression of nesfatin-1 protein and NUCB2 mRNA was detected in the immortalized normal human bronchial cell line BEAS-2B and the non-small-cell lung cancer cell line H1299. Immunohistochemical staining revealed the localization of nesfatin-1 binding sites in both cell lines. Nesfatin-1 treatment significantly increased the proliferation and migration of BEAS-2B cells but not of H1299 cells. The expression levels of cell proliferation-related genes, such as TGFα, PXN, MTOR, and CCND1, were upregulated in BEAS-2B cells, with no significant changes observed in H1299 cells. In addition, phosphorylation of FAK, PI3 K, and AKT was increased in BEAS-2B cells, whereas only FAK phosphorylation was increased in H1299 cells. To further assess the role of endogenous nesfatin-1, NUCB2 expression was silenced using small interfering RNA. Knockdown of NUCB2 suppressed proliferation and migration of BEAS-2B cells, as well as their expression of TGFα, PXN, MTOR, and CCND1; however, it had no significant effect on H1299 cells. These results suggest that nesfatin-1 promotes proliferation and migration in normal lung epithelial cells but not in lung cancer cells. Further research is needed to elucidate the molecular mechanisms underlying the differential effects of nesfatin-1 on normal and cancerous lung cells.