Background
Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor in East Asia. Emerging evidence indicated that long intergenic non-coding RNA 152 (LINC00152) acts as an oncogene in many types of cancers including ESCC. This study aims to identify the biological mechanisms of LINC00152 in ESCC, hinting for new therapeutic target for ESCC patients.
Conclusion
In this study, we found that LINC00152 modulated Rab10 to promote cell proliferation, migration and invasion in ESCC by sponging miR-107. This new regulatory network may provide a novel therapeutic target for ESCC patients.
Methods
The levels of LINC00152, microRNA-107 (miR-107) and Ras-related protein Rab-10 (Rab10) were measured in ESCC tissues and cells using qRT-PCR. The protein level of Rab10 was measured by Western blot assay. The putative target of LINC00152 or miR-107 was searched using starBase v2.0 and TargetScan online databases, and dual-luciferase reporter assay was conducted to detect the interaction between miR-107 and LINC00152 or Rab10. The cell viability was monitored by CCK8 assay, and the abilities of migration and invasion were assessed by Transwell assay, respectively. The mice model experiments were constructed to affirm the biological role of LINC00152 in vivo.
Results
LINC00152, Rab10 was significantly upregulated, and miR-107 was strikingly down-regulated in ESCC tissues and cell lines (TE-1 and KYSE30). LINC00152 was verified as a sponge for miR-107, and Rab10 was a direct target of miR-107. LINC00152 depletion decreased cell viability and abilities of migration and invasion by regulating miR-107 in vitro and blocked xenograft tumor growth in vivo. The overexpression of miR-107 reduced cell viability and the abilities of migration and invasion by modulating Rab10. LINC00152 positively regulated Rab10 expression by sponging miR-107.