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miR-613 inhibits bladder cancer proliferation and migration through targeting SphK1
Haifeng Yu1, Ping Duan2, Haibo Zhu1
1Department of Urology, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou 325000, Zhejiang, China.
Objectives:
Increasing evidence has suggested that microRNA (miRNA) dysregulation may contribute to tumor progression and metastasis. However, the role of miR-613 in bladder cancer was still unknown.
Materials And Methods:
qRT-PCR and Western blotting were performed to detect the expression of miR-613 and its direct target gene. CCK-8 analysis, qRT-PCR and cell invasion were performed to measure the cell function.
Results:
We demonstrated that the expression of miR-613 was downregulated in the bladder cancer cell lines. In addition, miR-613 expression was downregulated in the bladder cancer tissues compared to the adjacent normal tissues. Out of 35 bladder cancer tissues, miR-613 was downregulated in 27 cases compared to the adjacent tissues. Ectopic expression of miR-613 suppressed the bladder cancer cell proliferation and invasion. Moreover, miR-613 overexpression enhanced the expression of epithelial biomarker, Ecadherin, and suppressed the expression of mesenchymal biomarker, Vimentin, Snail and N-cadherin. Furthermore, we identified the Sphingosine kinase 1 (SphK1) as the direct target gene of miR-613 in the bladder cancer cell. Restoration of Sphk1 partially rescued miR-613-inhibited bladder cancer cell proliferation, invasion and EMT.
Conclusions:
These data suggested that miR-613 acted a tumor suppressive role in bladder cancer through targeting SphK1 in bladder.
Insights
MicroRNA-613 (miR-613) is downregulated in bladder cancer, suppressing tumor growth and metastasis. Targeting Sphingosine kinase 1 (SphK1) by miR-613 inhibits cancer cell proliferation and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA (miRNA) dysregulation is implicated in cancer progression.
- The specific role of miR-613 in bladder cancer remains uncharacterized.
Purpose of the Study:
- To investigate the expression and function of miR-613 in bladder cancer.
- To identify the molecular targets of miR-613 in this disease.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting were used to assess miR-613 and SphK1 expression.
- Cell proliferation (CCK-8 assay) and invasion assays were performed to evaluate cellular functions.
- Epithelial-mesenchymal transition (EMT) markers were analyzed following miR-613 overexpression.
Main Results:
- miR-613 expression was significantly downregulated in bladder cancer cell lines and tissues.
- Overexpression of miR-613 inhibited bladder cancer cell proliferation and invasion.
- miR-613 suppressed EMT by upregulating E-cadherin and downregulating Vimentin, Snail, and N-cadherin.
- Sphingosine kinase 1 (SphK1) was identified as a direct target of miR-613.
- Restoration of SphK1 partially reversed the suppressive effects of miR-613 on bladder cancer cells.
Conclusions:
- miR-613 functions as a tumor suppressor in bladder cancer.
- The tumor-suppressive role of miR-613 is mediated through the inhibition of SphK1 and EMT.