Salidroside suppresses nonsmall cell lung cancer cells proliferation and migration via microRNA-103-3p/Mzb1.

Abstract

Lung cancer is the leading cause of cancer death in both men and women in the worldwide. Metastasis is the leading cause of cancer mortality and is a major hurdle for lung cancer treatment. Salidroside, a glycoside of tyrosol, is isolated from Rhodiola rosea and shows anticancer functions in several cancers. Recently, studies have reported that salidroside could inhibit the proliferation and metastasis of lung cancer; however, we need to explore further mechanism to provide evidence for clinical treatment. MicroRNAs (miRNAs) are regulatory molecules frequently aberrantly expressed in cancers, and a key role in carcinogenesis through regulation of their target genes. Consistent with previous reports, we found that salidroside could inhibit the proliferation of nonsmall cell lung cancer (NSCLC) cells, and elevated the level of miR-103-3p. Furthermore, we showed that the level of miR-103-3p was significantly downregulated in NSCLC tissues and NSCLC cell lines A549 and H460 and was significantly correlated with NSCLC proliferation and metastasis. Further studies indicated that an endoplasmic reticulum calcium regulator Mzb1 (marginal zone B and B-1 cell-specific protein) was a direct target gene of miR-103-3p, evidenced by the direct binding of miR-103-3p with the 3' untranslated region of Mzb1. We have also shown that overexpressing Mzb1 was able to inhibit the suppression effect of miR-103-3p on A549 migration and metastasis. These results demonstrate that salidroside suppresses NSCLC proliferation and metastasis by regulating miR-103-3p/Mzb1.