RETRACTED ARTICLE: Downregulation of monocarboxylate transporter 1 inhibits the invasion and migration through suppression of the PI3K/Akt signaling pathway in human nasopharyngeal carcinoma cells

Zhang, Pei; Ma, Jun; Gao, Junying; Liu, Fang; Sun, Xiaojin; Fang, Fang; Song, Zhao; Liu, Hao

doi:10.1007/s10863-018-9763-y

Cited by 14 publications

(11 citation statements)

References 33 publications

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“…PI3K/AKT pathway is one of the most common oncogenic signaling cascades whose aberrant regulation affects many cellular processes in a range of human cancers [44]. For instance, suppression of the PI3K/Akt signaling pathway by down-regulating monocarboxylate transporter 1 inhibits the invasion and migration in human nasopharyngeal carcinoma cells [45]. Herein, we found unsurprisingly that knockdown of TP73-AS1 could inactivate this pathway in LAD cells and confirmed that TP73-AS1 play an oncogenic role in LAD through activating this pathway.…”

Section: Discussionmentioning

confidence: 99%

LncRNA TP73-AS1 promoted the progression of lung adenocarcinoma via PI3K/AKT pathway

et al. 2019

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Lung adenocarcinoma (LAD) is one of the most common malignancies that threats human health worldwide. Long non-coding RNAs (lncRNAs) have been reported to play significant roles in tumorigenesis and might be novel biomarkers and targets for diagnosis and treatment of cancers. TP73-AS1 is a newly discovered lncRNA involved in the tumorigenesis and development of several cancers. However, its role in LAD has not been investigated yet. In the present study, we first found that TP73-AS1 expression was markedly increased in LAD tissues and cell lines and its overexpression was strongly associated with poor clinical outcomes. Then the loss/gain-of-function assays elucidated that TP73-AS1 contributed to cell proliferation, migration, and invasion in vitro, and the in vivo experiments illustrated that its knockdown inhibited tumor growth and metastasis. What was more, we discovered that phosphoinositide 3-kinase and AKT (PI3K/AKT) pathway was activated both in LAD tissues and cell lines but inactivated under TP73-AS1 silence. Moreover, the activation of this pathway could rescue the inhibitory effects of TP73-AS1 suppression on LAD cellular processes partially. These data suggested that TP73-AS1 served as an oncogene in LAD partially through activating PI3K/AKT pathway and it could be a potential target for diagnosis and treatment of LAD.

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Section: Discussionmentioning

confidence: 99%

LncRNA TP73-AS1 promoted the progression of lung adenocarcinoma via PI3K/AKT pathway

et al. 2019

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“…These effects are mediated by multiple mechanisms, including hexokinase expression. 13 Furthermore, there is a functional link between Akt-mTOR activation and MCT-1 expression 41 and possibly between Akt and the pentose phosphate pathway. 42 For these reasons, we performed an additional clustering analysis to subclassify our patients based on the insulin-induced phosphorylation of Akt and its immediate downstream mediator mTOR.…”

Section: Discussionmentioning

confidence: 99%

Effects of insulin and pathway inhibitors on the PI3K-Akt-mTOR phosphorylation profile in acute myeloid leukemia cells

Nepstad

Hatfield

Grønningsæter

et al. 2019

Sig Transduct Target Ther

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The phosphatidylinositol 3-kinase (PI3K)-Akt-mechanistic target of rapamycin (mTOR) pathway is constitutively activated in human acute myeloid leukemia (AML) cells and is regarded as a possible therapeutic target. Insulin is an agonist of this pathway and a growth factor for AML cells. We characterized the effect of insulin on the phosphorylation of 10 mediators in the main track of the PI3K-Akt-mTOR pathway in AML cells from 76 consecutive patients. The overall results showed that insulin significantly increased the phosphorylation of all investigated mediators. However, insulin effects on the pathway activation profile varied among patients, and increased phosphorylation in all mediators was observed only in a minority of patients; in other patients, insulin had divergent effects. Global gene expression profiling and proteomic/phosphoproteomic comparisons suggested that AML cells from these two patient subsets differed with regard to AML cell differentiation, transcriptional regulation, RNA metabolism, and cellular metabolism. Strong insulin-induced phosphorylation was associated with weakened antiproliferative effects of metabolic inhibitors. PI3K, Akt, and mTOR inhibitors also caused divergent effects on the overall pathway phosphorylation profile in the presence of insulin, although PI3K and Akt inhibition caused a general reduction in Akt pT308 and 4EBP1 pT36/pT45 phosphorylation. For Akt inhibition, the phosphorylation of upstream mediators was generally increased or unaltered. In contrast, mTOR inhibition reduced mTOR pS2448 and S6 pS244 phosphorylation but increased Akt pT308 phosphorylation. In conclusion, the effects of both insulin and PI3K-Akt-mTOR inhibitors differ between AML patient subsets, and differences in insulin responsiveness are associated with differential susceptibility to metabolic targeting.

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“…Cells were homogenized and lysed with cell lysis buffer containing protease and phosphatase cocktail inhibitors (Sigma-Aldrich). A total of 20 mg lysates were separated on 10% SDS-PAGE and transferred to PVDF membranes (Bio-Rad Laboratories) [14]. After blocked with 5% non-fat milk in in tris-buffered saline tween-20, membranes were incubated with primary antibodies overnight at 4 C and horseradish peroxidase-conjugated secondary antibodies for additional 2 h. Blots were developed by enhanced chemiluminescence (Santa Cruz Biotechnology, Santa Cruz, USA).…”

Section: Western Blot Analysismentioning

confidence: 99%

Montelukast promotes mitochondrial biogenesis via CREB/PGC-1α in human bronchial epithelial cells

Wang

Cheng

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Bronchial epithelial mitochondrial dysfunction including impaired mitochondrial biogenesis has been linked with the initiation and development of bronchial asthma. Montelukast, a robust antagonist of cysteinyl leukotriene receptors, has been widely applied for the therapies of bronchial asthma. However, the effects of montelukast in airway epithelial mitochondrial dysfunction are less reported. In the present study, we report that montelukast treatment in human bronchial epithelial cells of Beas-2b increased the expressions of PGC-1a, NRF-1 and TFAM. As expected, montelukast promoted mitochondrial biogenesis in Beas-2b cells through increasing mitochondrial mass, mtDNA/nDNA and the expression of cytochrome B. Importantly, we found that montelukast caused a functional gain in mitochondria of Beas-2b cells. Mechanistically, we found that montelukast treatment increased intracellular cAMP levels and activation of CREB. Blockage of CREB with H89 abolished montelukast-induced expression of PGC-1a. These findings report a novel pharmacological function of montelukast in stimulating mitochondrial biogenesis in Beas-2b cells, mediating by the CREB/PGC-1a pathway.

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RETRACTED ARTICLE: Downregulation of monocarboxylate transporter 1 inhibits the invasion and migration through suppression of the PI3K/Akt signaling pathway in human nasopharyngeal carcinoma cells

Cited by 14 publications

References 33 publications

LncRNA TP73-AS1 promoted the progression of lung adenocarcinoma via PI3K/AKT pathway

LncRNA TP73-AS1 promoted the progression of lung adenocarcinoma via PI3K/AKT pathway

Effects of insulin and pathway inhibitors on the PI3K-Akt-mTOR phosphorylation profile in acute myeloid leukemia cells

Montelukast promotes mitochondrial biogenesis via CREB/PGC-1α in human bronchial epithelial cells

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