LncPTEN1, a long non-coding RNA generated from PTEN, suppresses lung cancer metastasis through the regulation of EMT progress

Lung cancer is among the most frequently observed and lethal malignancies globally, and metastasis represents a critical determinant of patient outcomes. PTEN, a well-established tumor suppressor, has emerged as an important regulator in lung cancer progression. However, the molecular mechanism of <i>PTEN</i> gene suppressing lung cancer metastasis lacks deeper exploration. In this research, we identify and characterize LncPTEN1, a novel long non-coding RNA generated from <i>PTEN</i> gene. We show that YTHDC1 promotes the alternative splicing of LncPTEN1, resulting in significantly elevated LncPTEN1 expression in normal lung cells. Clinical analyses across multiple patient cohorts demonstrate that low LncPTEN1 expression strongly correlates with poor patient survival and increased metastasis, indicating its potential as a prognostic biomarker. Mechanistically, LncPTEN1 facilitates the interaction between Trim16 and Vimentin, promoting the ubiquitination and proteasomal degradation of Vimentin, thereby suppressing EMT-driven metastasis. The collective evidence from our investigation demonstrates that LncPTEN1 represents a novel tumor-suppressive lncRNA which inhibits lung cancer metastasis through promoting the degradation of Vimentin and inhibiting the EMT progress.