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)

Numerous studies have demonstrated that microRNAs (miRs) are involved in several physiological and pathological processes, and participate in cancer initiation and progression. The abnormal expression of miR-150 has been reported in numerous types of human cancer. However, at present there are no studies of miR-150 in osteosarcoma (OS). Reverse transcription-quantitative polymerase chain reaction was performed to measure miR-150 expression levels in OS tissues and cell lines. Subsequent to transfection with miR-150 mimics or zinc finger E-box binding homeobox 1 (ZEB1) small interfering RNA, an MTT assay, Transwell migration and invasion assays, western blotting and a Dual-Luciferase reporter assay were performed in human OS cell lines. The present study revealed that miR-150 was downregulated in OS tissues and cell lines. In addition, the expression levels of miR-150 were correlated with the clinical stage and degree of distant metastasis of patients with OS. In addition, ZEB1 was identified as a direct target of miR-150 in vitro. In conclusion, miR-150 targeted ZEB1 to function as an antioncogenic regulator in OS. These findings elucidated a novel underlying mechanism for the pathogenic process in OS carcinogenesis and progression, and may provide novel targeted therapeutic regimens for patients with OS.
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PMID:MicroRNA-150 functions as an antioncogenic regulator in osteosarcoma. 2878 86

Naringin, a citrus bioflavonoid, has anti-inflammatory actions and cardio- and neuroprotective effects. In addition, naringin exhibits multiple antitumor actions in several cancer types, including osteosarcoma, the most common type of bone cancer. Here, we show that naringin inhibits proliferation and invasion and induces apoptosis in human osteosarcoma cells by inhibiting zinc finger E-box binding homeobox 1 (Zeb1), a transcriptional repressor of epithelial differentiation involved in tumor metastasis. Our expression analyses confirm that Zeb1 is highly expressed in osteosarcoma specimens and cell lines. The effects of naringin, which included downregulation of Cyclin D1, MMP2, and bcl-2, where reproduced by siRNA-mediated Zeb1 silencing, whereas Zeb1 overexpression increased proliferation, migration, and Cyclin D1, MMP2, and bcl-2 levels. In addition, naringin administration reduced tumor nodule formation and attenuated the expression of the above proteins in the livers of mice injected with MG63 osteosarcoma cells. Our study provides preclinical evidence for the potential therapeutic application of naringin in the treatment of osteosarcoma.
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PMID:Naringin targets Zeb1 to suppress osteosarcoma cell proliferation and metastasis. 3058 Mar 26

Long non-coding RNAs (LncRNAs), are significant in a number of biological stages and illnesses. The myocardial infarction associated transcript (MIAT) serves a function in numerous types of illness and physiological and pathological processes, including paranoid schizophrenia, diabetic retinopathy, myocardial infarction and neuroendocrine prostate cancer. However, the function of the lncRNA MIAT in the development of osteosarcoma is unknown. It has been identified that during the development of osteosarcoma, MIAT is upregulated in tumor tissues compared to adjacent non-tumor tissues. The spreading and proliferation of osteosarcoma cells was reduced by MIAT knockdown. These findings indicate that MIAT functions by competing with critical RNAs to target miR-150-5p and activate zinc finger E-box binding homeobox 1 to modulate the function of osteosarcoma cells. Together, the present findings may contribute to the understanding of the pathogenesis of osteosarcoma.
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PMID:Long non-coding RNA MIAT competitively binds miR-150-5p to regulate ZEB1 expression in osteosarcoma. 3065 89

Small nucleolar RNA host gene 3 (SNHG3), a long noncoding RNA (lncRNA), acts as an oncogene in hepatocellular carcinoma (HCC), whereas microRNA (miR)-326 plays an inhibitory role in some types of human cancers, including melanoma, osteosarcoma, and gastric cancer. In the present study, by analyzing 47 tissue specimens of human HCC, we found that the relative expression levels of SNHG3 were significantly higher in HCC tissues than those in the adjacent noncancerous tissues, whereas the relative expression levels of miR-326 were significantly lower in HCC tissues. Furthermore, the relative mRNA levels of Sma and Mad Related Family 3 (SMAD3) and zinc finger E-box binding homeobox 1 (ZEB1) were significantly higher in HCC tissues compared with the adjacent noncancerous tissues. In human HCC cell lines, SNHG3 overexpression promoted the proliferation, migration, and epithelial-mesenchymal transition and inhibited apoptosis, whereas knockdown of SNHG3 expression exerted the opposite effects. Importantly, miR-326 or miR-326 inhibitor restored the aforementioned effects of SNHG3 overexpression or SNHG3 knockdown. We thus found that the miR-326-response element is present in SNHG3 and the 3'-untranslated region of SMAD3 mRNA. In fact, SNHG3 overexpression increased the expression levels of SMAD3 and ZEB1, while miR-326 decreased the expression levels of SMAD3. These results suggest that SNHG3 may function as a competing endogenous RNA (ceRNA) for miR-326, which in turn enhances SMAD3 and ZEB1 expression. In conclusion, we propose that SNHG3 promotes HCC progression via the miR-326/SMAD3/ZEB1 signaling pathway. The findings may provide novel targets for the diagnosis and treatment of HCC.
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PMID:LncRNA SNHG3 Promotes Hepatocellular Tumorigenesis by Targeting miR-326. 3154 93