POSTN promotes the progression of NSCLC via regulating TNFAIP6 expression

Aberrant upregulation of Periostin (POSTN) expression has been implicated in various disease-related pathological cascades, notably inflammatory responses, fibrotic processes and tumor progression, including non-small cell lung cancer (NSCLC). The present study aimed to elucidate the functional role and underlying mechanisms of POSTN in NSCLC. Immunohistochemical and Western blot analysis consistently revealed elevated POSTN levels in NSCLC tissues and cell lines. POSTN expression negatively correlated with patient prognosis. Functional experiments utilizing POSTN-targeting siRNAs demonstrated a significant suppression of NSCLC cell proliferation, epithelial-to-mesenchymal transition (EMT), migration and invasion, whereas POSTN overexpression via plasmid transfection enhanced these oncogenic properties. Mechanistically, RNA sequencing analysis and subsequent validation studies revealed that POSTN positively modulates the transcriptional expression of tumor necrosis factor alpha-induced protein 6 (TNFAIP6) in NSCLC. Notably, a positive correlation was observed between POSTN and TNFAIP6 expression levels, and their overexpression positively correlated with NSCLC progression. Furthermore, TNFAIP6 overexpression rescued the inhibitory effects of POSTN knockdown on NSCLC malignant phenotypes. Collectively, our findings indicate that POSTN promotes NSCLC malignancy through TNFAIP6 upregulation, positioning POSTN as a promising biomarker and potential therapeutic target for NSCLC prognosis and treatment strategies in clinical settings. •POSTN upregulation in NSCLC tissues links to poor prognosis.•.POSTN knockdown reduces NSCLC malignancy; overexpression enhances it.•.POSTN regulates TNFAIP6 in NSCLC, showing a positive correlation.•.POSTN drives NSCLC malignancy, marking it as a biomarker and therapeutic target.