Abstract
Melanoma is the deadliest cutaneous neoplasm. To prevent metastasis, early diagnosis and surgical treatment is vital. Long non-coding RNAs (lncRNAs) may serve as biomarkers and therapeutic targets in tumors. We investigated the molecular mechanisms of lncRNA KCNQ1OT1 in melanoma. Real time PCR demonstrated that KCNQ1OT1 expression is up-regulated in melanoma tissues and cells. KCNQ1OT1 promoted cell proliferation and metastasis in melanoma. By directly bindin to miR-153, KCNQ1OT1 acted as a competing endogenous RNA (ceRNA) to de-repress MET expression. Our results may provide the basis for a novel strategy for early detection and/or treatment of melanoma.
Highlights
The incidence and mortality rate of melanoma continues to increase despite advances in drug discovery programs and molecular approaches for identifying drug targets [1]
To identify Long non‐coding RNAs (lncRNAs) involved in melanoma, we performed a cDNA microarray analysis
We demonstrated that KCNQ1OT1 was upregulated in melanoma tissues and cells
Summary
The incidence and mortality rate of melanoma continues to increase despite advances in drug discovery programs and molecular approaches for identifying drug targets [1]. In order to effectively treat melanoma, it is necessary to inhibit key mechanistic events which regulate melanoma development, including cell proliferation, survival, angiogenesis, invasion, and metastasis [2]. C-Met is a receptor tyrosine kinase (RTK) that promotes the growth, metastasis, and angiogenesis of melanoma cells. The combination of vemurafenib and METtargeting siRNA can inhibit cell growth and reduce cell invasion and migration by melanoma cells with MET amplification [3]. Melanoma is sensitive to c-Met inhibition, which decreases Akt phosphorylation, tumor cell proliferation, migration, and induction of apoptosis. Melanoma progression is stimulated by c-Met activation
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