Leptin-mediated ERK Signaling Pathway Promotes the Transformation 
of Rat Alveolar Type II Epithelial Cells Induced by Yunnan Tin Mine Dust

This study aims to investigate the involvement of leptin-mediated extracellular regulated protein kinase (ERK) signaling pathway in the malignant transformation of rat alveolar type II epithelial cells induced by Yunnan tin mine dust. Methods Immortalized rat alveolar cells type II (RLE-6TN) cells were infected with Yunnan tin mine dust at a concentration of 200 μg/mL for nine consecutive generations to establish the infected cell model, which was named R200 cells. The cells were cultured normally, named as R cells. The expression of leptin receptor in both cell groups was detected using the Western blot method. The optimal concentration of leptin and mito gen-activated protein kinase kinase (MEK) inhibitor (U0126) on R200 cells was determined using the MTT method. Starting from the 20th generation, the cells in the R group were co-cultured with leptin, while the cells in the R200 group were co-cultured with the MEK inhibitor U0126. The morphological alterations of the cells in each group were visualized utilizing hematoxylin-eosin staining. Additionally, concanavalin A (ConA) was utilized to detect any morphological differences, and an anchorage-independent growth assay was conducted to assess the malignant transformation of the cells. The chan ges in the ERK signaling pathway in epithelial cells after the action of leptin were detected using the Western blot method. Results Both the cells in the R group and R200 group express leptin receptor OB-R. Compared to the R200 grou...
Source: Chinese Journal of Lung Cancer - Category: Cancer & Oncology Source Type: research