Delving into the Latest Updates on SOL-587 with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Target-

Mechanism-

Therapeutic Areas

Neoplasms

Active Indication-

Inactive Indication

Neoplasms

Originator Organization

Sentinel Oncology Ltd.

Active Organization-

Inactive Organization

Sentinel Oncology Ltd.

Drug Highest PhasePendingPreclinical

First Approval Date-

Regulation-

OBJECTIVEThis study aims to explore the cancer-associated functions of microRNA-587 (miR-587) in the development of non-small-cell lung carcinoma (NSCLC) and the molecular mechanism.PATIENTS AND METHODSRelative expression levels of miR-587 and CYLD in NSCLC samples were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Proliferative and migratory abilities in A549 and H1299 cells with overexpressed miR-587 were examined by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. The regulatory interaction between miR-587 and CYLD was determined by Dual-Luciferase reporter assay and Pearson correlation test. At last, the co-regulation of miR-587 and CYLD on NSCLC cell functions was assessed by rescue experiments.RESULTSMiR-587 was upregulated in NSCLC samples and closely linked to tumor staging, whereas CYLD was downregulated and negatively correlated to that of miR-587. Survival analysis suggested that miR-587 was an unfavorable factor to the prognosis of NSCLC. Overexpression of miR-587 stimulated proliferative and migratory abilities in A549 and H1299 cells. CYLD was the downstream gene binding miR-587. Overexpression of CYLD could partially abolish the regulatory effects of overexpressed miR-587 on promoting proliferative and migratory abilities in NSCLC cells.CONCLUSIONSMiR-587 stimulates proliferative and migratory abilities in NSCLC by downregulating CYLD, thus aggravating the progression of NSCLC.

100 Deals associated with SOL-587

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