LINC00888 Promotes Gastric Cancer Growth and Metastasis by Sponging miR-145-5p to Regulate FZD7 Expression.

INTRODUCTION

To investigate the clinical relevance, biological function, and molecular mechanisms of the long non-coding RNA LINC00888 in gastric cancer (GC).

METHODS

Expression profiles of LINC00888 were analyzed using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Associations with clinical features-including age, sex, tumor stage, recurrence, and survival were examined. Potential downstream targets were predicted using bioinformatics, and experimental validation was performed in GC cell lines via qRT-PCR, Western blot, and luciferase reporter assays. Functional roles were assessed by proliferation and invasion assays.

RESULTS

LINC00888 was upregulated in GC tissues and cell lines and associated with advanced stage, recurrence, and poor prognosis. Knockdown of LINC00888 reduced cell proliferation and invasion in vitro. Bioinformatics and experimental analyses indicated that LINC00888 may act as a competing endogenous RNA for miR-145-5p, potentially influencing Frizzled-7 (FZD7) expression.

DISCUSSION: LINC00888 promotes gastric cancer progression by modulating the miR-145- 5p/FZD7 axis and is associated with poor prognosis. It may serve as a prognostic biomarker and potential therapeutic target in GC. Integration of molecular biomarkers like LINC00888 into emerging IoT-based clinical platforms may further enhance personalized cancer management.

CONCLUSION

LINC00888 promotes GC progression via the miR-145-5p/FZD7 ceRNA network and may serve as a prognostic biomarker and therapeutic target.