Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increasing reports demonstrated that miRNAs play a critical role in tumor development and progression. Previous studies revealed that miR-1301 was abnormally expressed in various cancers. However, its function and underlying mechanism in osteosarcoma (OS) remains unknown. In this study, miR-1301 expression was significantly down-regulated in both OS tissues and cell lines. Down-regulated miR-1301 was obviously associated with malignant clinical features and poor overall survival of OS patients. miR-1301 overexpression inhibited cell proliferation, migration and invasion. In addition, we identified BCL9 act as a direct target of miR-1301 by directly binding to its 3'-UTR. In clinical OS tissues, miR-1301 negatively correlated BCL9 expression. BCL9 was up-regulated in OS tissues and cells. BCL9 overexpression promoted OS progression. Moreover, restoration of BCL9 expression at least partially abolished the proliferation, migration and invasion of miR-1301 on OS cells. In conclusion, our data indicated that miR-1301 inhibited cell proliferation, migration and invasion of OS by targeting BCL9, and may represent a novel potential therapeutic target and prognostic marker for OS.
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PMID:MicroRNA-1301 inhibits migration and invasion of osteosarcoma cells by targeting BCL9. 3017 67

Long non-coding RNAs (lncRNAs) play a key role in regulating tumor growth and metastasis of osteosarcoma (OS). Recent studies have reported that lncRNA small nucleolar RNA host gene 16 (SNHG16) is highly expressed in OS tissues and contributes to the proliferation, migration and invasion of OS cells. However, the molecular mechanism involved in the oncogenic role of SNHG16 in OS remains poorly known. In the current study, we confirmed that SNHG16 expression was markedly up-regulated in OS tissues compared to paracancerous tissues. The elevated level of SNHG16 closely associated with advanced tumor stages, larger tumor size and more distance metastasis. Furthermore, OS patients with high SNHG16 level had a significant poorer overall survival compared to patients with low SNHG16 level. Knockdown of SNHG16 suppressed the proliferation, migration and invasion of U2OS and MG63 cells. Mechanistically, SNHG16 acted as a competing endogenous RNA (ceRNA) by directly interacting with miR-1301 and inversely regulated its abundance in OS cells. Notably, suppression of miR-1301 rescued SNHG16 knockdown attenuated OS cell proliferation, migration and invasion. SNHG16 knockdown reduced the expression of BCL9 protein in OS cells. Accordingly, BCL9 restoration facilitated the proliferation, migration and invasion of OS cells with SNHG16 knockdown. Collectively, these results suggest that SNHG16 is a potential prognostic biomarker for OS patients. SNHG16 promotes BCL9 expression by sponging miR-1301 to facilitate the proliferation, migration and invasion of OS cells.
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PMID:LncRNA SNHG16 promotes proliferation, migration and invasion of osteosarcoma cells by targeting miR-1301/BCL9 axis. 3090 41