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Source: European Review for Medical and Pharmacological Sciences
Cancer: Adenocarcinoma
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Total 38 results found since Jan 2013.
OTX1 is a novel regulator of proliferation, migration, invasion and apoptosis in lung adenocarcinoma.
CONCLUSIONS: Silencing the OTX1 gene suppressed the proliferation, migration and invasion of NCI-H292 and XWLC cells, impeded the cell cycle transition from G2 to M phase, and accelerated apoptosis, revealing OTX1, a regulator of NSCLC, as a potential new therapeutic target.
PMID: 33015792 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - October 7, 2020 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
LncRNA MALAT1 knockdown alleviates myocardial apoptosis in rats with myocardial ischemia-reperfusion through activating PI3K/AKT signaling pathway.
CONCLUSIONS: The MALAT1 knockdown can markedly improve the I/R-induced myocardial injury and promote the cardiac function of rats, whose mechanism may be related to the activation of the AKT signaling pathway by MALAT1 siRNA. Therefore, lncRNA MALAT1 is expected to be a new therapeutic target for myocardial I/R injury.
PMID: 31841208 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - December 18, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
Effects of lncRNA MALAT1-mediated β-catenin signaling pathway on myocardial cell apoptosis in rats with myocardial ischemia/reperfusion injury.
CONCLUSIONS: MALAT1 knockdown can significantly ameliorate the I/R-induced myocardial injury and improve the cardiac function of the rats, whose mechanism is probably correlated with the inhibition of MALAT1 siRNA on β-catenin. Therefore, MALAT1 siRNA is expected to become a new target for the treatment of myocardial infarction.
PMID: 31773707 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - November 28, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
LncRNA MALAT1 affects high glucose-induced endothelial cell proliferation, apoptosis, migration and angiogenesis by regulating the PI3K/Akt signaling pathway.
CONCLUSIONS: Inhibiting lncRNA MALAT1 can promote endothelial cell proliferation, migration and angiogenesis and repress endothelial cell apoptosis simultaneously, whose mechanism may be related to the activation of the PI3K/Akt signaling pathway.
PMID: 31646587 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - October 26, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
LncRNA MALAT1 inhibits osteogenic differentiation of mesenchymal stem cells in osteoporosis rats through MAPK signaling pathway.
CONCLUSIONS: LncRNA MALAT1 was lowly expressed in OP rats. Moreover, it inhibited osteogenic differentiation of BMSCs by enhancing the activation of the MAPK signaling pathway, thereby promoting OP progression.
PMID: 31210287 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - June 20, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
Influence of lncRNA MALAT1 on septic lung injury in mice through p38 MAPK/p65 NF- κB pathway.
CONCLUSIONS: The knockdown of lncRNA MALAT1 can significantly improve the septic lung injury in mice, whose mechanism may be related to its inhibition on the p38 MAPK/p65 NF-κB signaling pathway.
PMID: 30779099 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - February 21, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
LncRNA SNHG8 promotes the development and chemo-resistance of pancreatic adenocarcinoma.
CONCLUSIONS: SNHG8 is highly expressed in pancreatic adenocarcinoma tissues and is negatively correlated with its prognosis. Moreover, SNHG8 promotes cell proliferation and cell cycle, whereas inhibits cell apoptosis and reduces the chemo-sensitivity of pancreatic adenocarcinoma cells.
PMID: 30556854 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - December 18, 2018 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
IL-6 induced lncRNA MALAT1 enhances TNF- α expression in LPS-induced septic cardiomyocytes via activation of SAA3.
CONCLUSIONS: IL-6 induced MALAT1 upregulation in cardiomyocytes in response to LPS treatment. MALAT1 can enhance TNF-α expression at least partly via SAA3 in LPS-treated cardiomyocytes. MALAT1 upregulation is a mechanism of cardiomyocyte death in response to the LPS stimulation.
PMID: 28165557 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - February 8, 2017 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
