LINC00467 promotes non-small-cell lung cancer progression by regulating PABPC1 stability which accompanied by changes in Wnt/β-catenin pathway activity.

Long non-coding RNA LINC00467 exerts a significant impact on various cancer types. However, its precise role in non-small-cell lung cancer (NSCLC) is not fully elucidated. Thus, the current study investigated the potential mechanism by which LINC00467 contributes to the progression of NSCLC. RT-qPCR and fluorescence in situ hybridization (FISH) results showed that overexpression of LINC00467 is closely associated with malignant characteristics in NSCLC patients. It promoted NSCLC cell proliferation and metastasis in both cell culture and animal models. Co-immunoprecipitation (Co-IP) and Western blot results indicated that LINC00467 may enhance the proteasome-dependent degradation of PABPC1 by facilitating its interaction with the ubiquitin E3 ligase E4B. Furthermore, LINC00467 was observed to influence the activity of the Wnt/β-catenin signaling pathway, possibly by regulating PABPC1 stability in NSCLC cells. These findings suggest that LINC00467 may contribute to NSCLC progression through a mechanism involving PABPC1, with the potential to modulate the Wnt/β-catenin pathway. This regulatory axis may provide insight into future therapeutic targets for NSCLC.