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)

Two cell lines derived from a lung metastasis of a rat osteosarcoma were treated with cisplatin (CDDP) and two phosphonic acid compounds (AMDP, DADP), AMDP-treated cells showed a decrease in FDG uptake, CDDP and DADP resulted in an increase. A block in G2 or in S and G2 phase was seen after CDDP and AMDP treatment. The changes in the cell cycle fractions were not related to the changes in FDG uptake. Furthermore, the transcription of the glucose transporter and hexokinase genes were elevated in CDDP and decreased in AMDP treated cells. However, the changes in FDG uptake were not fully explained by changes at the transcriptional level. The total uptake of thymidine was elevated although the incorporation of thymidine into DNA decreased. In both cell lines the changes in FDG uptake correlated with the changes in thymidine incorporation into DNA (r = 0.95 and r = 0.83, respectively). Cells with an increased FDG uptake showed a weaker growth inhibition than cells with a decrease in FDG uptake.
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PMID:Metabolic and transcriptional changes in osteosarcoma cells treated with chemotherapeutic drugs. 923 33

Accumulating evidence has shown that PI3K/Akt pathway is frequently hyperactivated in osteosarcoma (OS) and contributes to tumor initiation and progression. Altered phenotype of glucose metabolism is a key hallmark of cancer cells including OS. However, the relationship between PI3K/Akt pathway and glucose metabolism in OS remains largely unexplored. In this study, we showed that elevated Hexokinase-2 (HK2) expression, which catalyzes the first essential step of glucose metabolism by conversion of glucose into glucose-6-phosphate, was induced by activated PI3K/Akt signaling. Immunohistochemical analysis showed that HK2 was overexpressed in 83.3% (25/30) specimens detected and was closely correlated with Ki67, a cell proliferation index. Silencing of endogenous HK2 resulted in decreased aerobic glycolysis as demonstrated by reduced glucose consumption and lactate production. Inhibition of PI3K/Akt signaling also suppressed aerobic glycolysis and this effect can be reversed by reintroduction of HK2. Furthermore, knockdown of HK2 led to increased cell apoptosis and reduced ability of colony formation; meanwhile, these effects were blocked by 2-Deoxy-d-glucose (2-DG), a glycolysis inhibitor through its actions on hexokinase, indicating that HK2 functions in cell apoptosis and growth were mediated by altered aerobic glycolysis. Taken together, our study reveals a novel relationship between PI3K/Akt signaling and aerobic glycolysis and indicates that PI3K/Akt/HK2 might be potential therapeutic approaches for OS.
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PMID:PI3K/Akt signaling mediated Hexokinase-2 expression inhibits cell apoptosis and promotes tumor growth in pediatric osteosarcoma. 2611 68

Osteosarcoma is an aggressive malignant neoplasm in teenagers and young adults. Long non-coding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) is considered as an oncogene in osteosarcoma. However, the mechanism of TUG1 in regulating osteosarcoma has not been fully understood. We aimed to investigate whether the metabolic alteration is involved in the effect of TUG1 on osteosarcoma cells. Herein, we found that TUG1 was overexpressed in osteosarcoma cells compared with the normal osteoblastic cell line. Knockdown of TUG1 inhibited glucose consumption, lactate production and cell viability of osteosarcoma cells. Overexpression of TUG1 induced cell viability, whereas the induction was attenuated by 2-DG. The aberrant expression of TUG1 markedly affected the expression of hexokinase-2 (HK2). Knockdown of HK2 weakened the effect of TUG1 overexpression on glycolysis in osteosarcoma cells. We concluded that glycolysis was involved in the effect of TUG1 on cell viability of osteosarcoma cells. HK2 might be an important molecule by which TUG1 affected the glycolysis.
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PMID:LncRNA TUG1 affects cell viability by regulating glycolysis in osteosarcoma cells. 2996 67