Drug resistance, cancer recurrence, and metastasis are all caused by cancer stem cells (CSCs). For a study, researchers sought to present the results of the initial investigation into Palladin expression and its effects on lung cancer stem cell-like characteristics.
To examine Palladin expression and its relationship to prognosis, tissue microarrays were employed. Palladin expression was examined using immunofluorescence (IF), flow fluorescence assay, and Western blot in 6 NSCLC cell lines. Drug resistance and cell phenotypes were assessed. To establish Palladin’s function in vivo, xenograft models were created.
Palladin was discovered to be significantly expressed in the cytoplasm, more especially in the cytomembrane of NSCLC, and its high expression is linked to a poor prognosis utilizing tissue microarrays. In spherical cells, palladin is abundantly expressed and concentrated. Studies conducted in vitro and in vivo revealed that Palladin increased stem cell-like characteristics such as cell survival, invasion, migration, capacity for self-renewal, resistance to taxol, and tumorigenicity. Palladin enhanced the accumulation of β-catenin and triggered Wnt/β-catenin signaling, according to a Western blot analysis. Tissue microarrays analysis further supported the positive relationship between Palladin and β-catenin. Inhibitors of the Wnt/β-catenin pathway prevented Palladin from increasing sphere formation.
Palladin may function as an oncogene by encouraging NSCLC cell tumorigenicity and CSC-like characteristics via the Wnt/β-catenin signaling pathway. Palladin was also shown to have the potential to serve as a cell surface marker for the detection of LCSCs. The findings offered a potential target for creating putative LCSC-targeted drugs.
Reference: onlinelibrary.wiley.com/doi/10.1002/cam4.5192
