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

Osteosarcoma is the most common primary malignant tumour of the bone. Although new therapies continue to be reported, osteosarcoma-related morbidity and mortality remain high. Modern medicine has greatly increased knowledge of the physiopathology of this neoplasm. Novel targets for drug development may be identified through an understanding of the normal molecular processes that are deeply modified in pathological conditions. The aim of the present study is to investigate, by immunohistochemistry, the localisation of different growth factors and of the proliferative marker Ki-67 in order to determine whether these factors are involved in the transformation of osteogenic cells and in the development of human osteosarcoma. We observed a general positivity for NGF - TrKA - NT3 - TrKC - VEGF in the cytoplasm of neoplastic cells and a strong expression for NT4 in the nuclear compartment. TGF-beta was strongly expressed in the extracellular matrix and vascular endothelium. BDNF and TrKB showed a strong immunolabeling in the extracellular matrix. Ki-67/MIB-1 was moderately expressed in the nucleus of neoplastic cells. We believe that these growth factors may be considered potential therapeutic targets in the treatment of osteosarcoma, although proof of this hypothesis requires further investigation.
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PMID:Growth factors, their receptor expression and markers for proliferation of endothelial and neoplastic cells in human osteosarcoma. 2406 59

Long non-coding RNA (LncRNA) brain-derived neurotrophic factor antisense (BDNF-AS) has been found to be down-regulated and function in a tumor suppressive role in human cancers. However, the expression status and function of BDNF-AS is still unknown in osteosarcoma (OS). In our study, BDNF-AS expression was found to be decreased in OS tissues and cells. Moreover, BDNF-AS low expression was correlated with advanced Enneking stage, large tumor size and poor prognosis in OS patients. The multivariate analysis suggested low expression of BDNF-AS was an independent unfavorable prognostic factor for overall survival in OS patients. The in vitro studies indicated that BDNF-AS overexpression inhibits OS cell proliferation and promotes cell apoptosis through regulating cleaved caspase-3. In conclusion, BDNF-AS serves as a tumor suppressive lncRNA in OS.
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PMID:LncRNA BDNF-AS is associated with the malignant status and regulates cell proliferation and apoptosis in osteosarcoma. 3035 34

MicroRNAs (miRNAs) are integrally involved in biological and pathobiological development. Many studies have demonstrated the abnormal expression of microRNA-496 (miR-496) in various human malignant tumors. The present study was designed to investigate the functions and the underlying mechanisms of miR-496 in osteosarcoma (OS) progression. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine the expression of miR-496 in OS tissues and cell lines. Luciferase activity was used to confirm the interaction between miR-496 and brain derived neurotrophic factor (BDNF), a downstream gene of miR-496. RT-qPCR was also used to quantify BDNF mRNA expression, and the BDNF protein expression level was detected by western blot analysis. In addition, the Cell Counting Kit-8 (CCK-8) was used to detect cell viability. The results revealed that the level of miR-496 expression was significantly reduced in osteosarcoma tissues and cell lines. BDNF was verified to be a direct target gene of miR-496 and was found to be negatively regulated by miR-496. Overall, it was demonstrated that miR-496 inhibits osteosarcoma cell proliferation via inhibition of BDNF. Thus, the miR-496/BDNF axis may be a novel strategy for the clinical treatment of OS.
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PMID:MicroRNA-496 suppresses tumor cell proliferation by targeting BDNF in osteosarcoma. 3201 Mar 18

Background: Acute treatment with the selective serotonin reuptake inhibitor (SSRI), fluoxetine (Flx), induces anxiety-like behavioral effects. The serotonin2A receptor (5-HT2A) is implicated in the modulation of anxiety-like behavior, however its contribution to the anxiogenic effects of acute Flx remains unclear. Here, we examined the role of the 5-HT2A receptor in the effects of acute Flx on anxiety-like behavior, serum corticosterone levels, neural activation and immediate early gene (IEG) expression in stress-responsive brain regions, using 5-HT2A receptor knockout (5-HT2A -/-) mice of both sexes. Methods: 5-HT2A -/- and wild-type (WT) male and female mice received a single administration of Flx or vehicle, and were examined for anxiety-like behavior, serum corticosterone levels, FBJ murine osteosarcoma viral oncogene homolog peptide (c-Fos) positive cell numbers in stress-responsive brain regions of the hypothalamus and prefrontal cortex (PFC), and PFC IEG expression. Results: The increased anxiety-like behavior and enhanced corticosterone levels evoked by acute Flx were unaltered in 5-HT2A -/- mice of both sexes. 5-HT2A -/- female mice exhibited a diminished neural activation in the hypothalamus in response to acute Flx. Further, 5-HT2A -/- male, but not female, mice displayed altered baseline expression of several IEGs (brain-derived neurotrophic factor (Bdnf), Egr2, Egr4, FBJ osteosarcoma gene (Fos), FBJ murine osteosarcoma viral oncogene homolog B (Fosb), Fos-like antigen 2 (Fosl2), Homer scaffolding protein (Homer) 1-3 (Homer1-3), Jun proto-oncogene (Jun)) in the PFC. Conclusion: Our results indicate that the increased anxiety and serum corticosterone levels evoked by acute Flx are not influenced by 5-HT2A receptor deficiency. However, the loss of function of the 5-HT2A receptor alters the degree of neural activation of the paraventricular nucleus (PVN) of the hypothalamus in response to acute Flx, and baseline expression of several IEGs in the PFC in a sexually dimorphic manner.
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PMID:5-HT2A receptor loss does not alter acute fluoxetine-induced anxiety and exhibit sex-dependent regulation of cortical immediate early gene expression. 3271 97

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA AFAP1-AS1 promoted osteosarcoma proliferation and invasion via upregulating BDNF, by B.-M. Zhao, F.-H. Cheng, L. Cai, published in Eur Rev Med Pharmacol Sci 2019; 23 (7): 2744-2749-DOI: 10.26355/eurrev_201904_17547-PMID: 31002124" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17547.
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PMID:Long noncoding RNA AFAP1-AS1 promoted osteosarcoma proliferation and invasion via upregulating BDNF. 3296 45