Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0029463 (
osteosarcoma
)
16,637
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Genetic factors influencing the pathogenesis of osteoporosis are still largely unknown. We employed genome-wide gene expression approach in order to discover novel genes involved in the pathogenesis of osteoporosis. To this end, primary cultures of osteoblasts isolated from osteoporotic and non-osteoporotic human bone tissue samples were prepared. One thousand six hundred six genes were found to be differentially expressed, indicating increased demand for protein synthesis and decreased cell proliferation rate in osteoblasts from osteoporotic tissue as compared to osteoblasts from non-osteoporotic tissue. At first, top four genes, based on the microarray data and potential role in bone metabolism, were further studied in bone tissue samples of 55 patients. PTN and COL15A1 were both downregulated in osteoporotic bone tissue (6.2- and 3.4-fold, respectively, both p<0.05), while IBSP and CXCL2 were both upregulated (5.7-fold, p<0.05, and 2.1-fold, p>0.05). Further biostatistical analysis of the microarray data by gene set enrichment analysis suggested oxidative stress may have an important part in the pathogenesis of osteoporosis. Thus, secondly, we tested it by an in vitro assay on human
osteosarcoma
cell line cells treated with hydrogen peroxide. After 72 h of treatment with 500 microM hydrogen peroxide, the upregulation of the same genes involved in the response to oxidative stress as on the microarrays was observed: MT1G (metallothionein 1G, 22.1-fold, p<0.05),
TXNRD1
(thioredoxin reductase 1, 3.7-fold, p<0.05), AOX1 (aldehyde oxidase 1, 24.5-fold, p<0.05) and GSR (glutathione reductase, 4.7-fold, p<0.05). Our results present a novel list of genes and metabolic pathways that may be associated with the pathogenesis of osteoporosis. PTN, CXCL2, COL15A1, IBSP, AOX1, MT1G, GSR and
TXNRD1
are candidate genes for further studies in the assessment of the genetic susceptibility to osteoporosis. In addition, differences in protein synthesis, cell proliferation rate and response to oxidative stress may also be involved in the pathogenesis of osteoporosis.
...
PMID:A microarray based identification of osteoporosis-related genes in primary culture of human osteoblasts. 1978 75
It was well established that long non-coding RNAs (LncRNAs) could serve as oncogene or tumor suppressor in terms of the tumor type. FTX, as a member of lncRNA family, has been reported to be associated with several tumor progressions, such as hepatocellular carcinoma (HCC), renal cell carcinoma (RCC) and colorectal cancer. However, the regulatory role of FTX in
osteosarcoma
(OS) still lacks research analysis. This paper aims to explore how FTX exerts its regulatory role on OS by modulating
TXNRD1
/miR-320a, so as to provide a novel lncRNA theoretical framework for the diagnosis and treatment of OS. QRT-PCR revealed that FTX and
TXNRD1
were abnormally upregulated in OS, whereas miR-320a expression was significantly decreased. Luciferase reporter analysis showed that both FTX and
TXNRD1
could combine with miR-320a. A series of functional experiments indicated that knockdown of FTX could suppress OS cell proliferation and migration, while facilitating apoptosis ability simultaneously. However,
TXNRD1
overexpression or miR-320a inhibition could rescue the oncogenic function of FTX. Taken all the experiment results together, this paper indicated that FTX impacted
osteosarcoma
cell proliferation and migration by modulating
TXNRD1
/miR-320a.
...
PMID:LncRNA FTX inhibition restrains osteosarcoma proliferation and migration via modulating miR-320a/TXNRD1. 3192 Jan 41