REDD1 Affects Proliferation, Apoptosis, Migration, and Colony Formation via p-ERK and p-JNK Signaling in Lung Adenocarcinoma Cells Under Hypoxia.

Background: Regulated in development and DNA damage response 1 (REDD1) is a stress-related protein that is found to be involved in tumor progression. The role and internal regulatory mechanism of REDD1 in lung adenocarcinoma (LUAD) remain unidentified as of yet. Methods: Immunohistochemical and Western blot tests were performed to evaluate REDD1 expression in LUAD tissues. EdU staining, cell counting kit-8 assays, and colony formation analyses were conducted to estimate cell proliferation. Flow cytometry was applied to examine apoptosis, while migration was detected by a transwell assay. Results: REDD1 was upregulated in LUAD tissues, and hypoxia promoted the expression of REDD1 in LUAD cells. In addition, knockdown of REDD1 inhibited the increase in proliferation, migration, and colony formation induced by hypoxia in LUAD cells. Apoptosis was decreased by hypoxia and restored after REDD1 downregulation. Furthermore, p-ERK and p-JNK signaling pathways were involved in the changes in proliferation, apoptosis, and migration of LUAD cells following REDD1 knockdown under hypoxia. Conclusions: REDD1 may be a possible therapeutic target for LUAD.