We are analyzing https://link.springer.com/article/10.1007/s11033-019-04929-x.

Title:
Targeting the phosphoinositide 3-kinase/AKT pathways by small molecules and natural compounds as a therapeutic approach for breast cancer cells | Molecular Biology Reports
Description:
The phosphoinositide 3-kinase/AKT/mTOR (PI3K/AkT/mTOR) pathway plays a pivotal role in the uncontrolled growth, migration and development of human breast cancer. The elevated expression of TGF-β1 increases the PI3K/AkT/mTOR activity in human breast cancer tissue and potentially motivates tumor metastasis and resistance to chemotherapy. Here, we investigated whether treatment with PI3K/AkT/mTOR dual inhibitor NVP-BEZ235 alone or in combination with caffeic acid phenyl ester (CAPE) could prevent TGF-β1 effects on breast cancer cells. MCF-7 human breast cancer cells were exposed to TGF-β1 for 14 days and then were treated with/without NVP-BEZ235 and/or CAPE. Cell viability, apoptosis, CXCR4 surface expression and mRNA levels of CXCR4 and TWIST-1 were analyzed in all treated groups. We found that treatment of human breast cancer cells with a combination of NVP-BEZ235 and CAPE increased induction of cellular death. Although flow cytometry analysis demonstrated that NVP-BEZ235 alone treatment reduced CXCR4 expression while increasing CXCR4 mRNA level; when NVP-BEZ235 was combined with CAPE, inhibition of CXCR4 surface expression and enhancement of CXCR4 mRNA expression was diminished. In addition, TWIST-1 mRNA expression was down regulated in samples treated with both NVP-BEZ235 and CAPE. These altogether signified that NVP-BEZ235 in combination with CAPE showed improved therapeutic efficacy in breast cancer cells by decreasing apoptotic resistance and reduction of CXCR4 and TWIST-1 expression at mRNA level could be one of mechanism of action.
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Keywords {🔍}

article, cancer, pubmed, google, scholar, cas, breast, expression, cells, nvpbez, cxcr, growth, tgfβ, central, human, res, shahrekord, pathway, cape, cell, access, research, molecular, inhibitor, acid, twist, university, medical, sciences, privacy, cookies, content, therapeutic, pikaktmtor, role, metastasis, dual, caffeic, ester, mrna, inhibition, transforming, biol, information, publish, search, kinaseakt, soltani, torki, increases,

Topics {✒️}

transforming growth factor-β1 transforming growth factor-β inhibiting pi3k/akt/xiap pathway triple-negative breast cancer epithelial–mesenchymal transition tgf-beta biology stromal-derived factor-1α dual pi3k-mtor inhibitor month download article/chapter mtor inhibitor nvp-bez235 pi3k/akt/mtor pathway rapamycin inhibitor nvp-bez235 phosphoinositide 3-kinase/akt/mtor integrin-dependent nuclear translocation tgf-β signaling axes pi3k/akt/mtor activity akt/pkb-mediated phosphorylation phosphoinositide 3-kinase/akt pathways molecular research center prevent tgf-β1 effects therapeutic target activates phosphatidylinositol 3-kinase barcellos-hoff mh pi3k/akt/mtor n-cadherin gene expression decreasing apoptotic resistance overcoming acquired resistance pi3k/mtor pathways full article pdf breast cancer metastasis breast cancer cells human breast cancer related subjects tgf-β1 increases increased oxidative stress privacy choices/manage cookies tgf-β family milad sabzevary ghahfarokhi medulloblastoma cell line mahdi ghatrehsamani prostate cancer invasion dual pi3k cape increased induction bmc cancer 10 cxcr4 surface expression metalloproteinases-3 gene expression cxcr4 mrna expression synergistic antitumor effect uncontrolled growth pi3k pathway

Questions {❓}

Harvey JR, Mellor P, Eldaly H et al (2007) Inhibition of CXCR28-mediated breast cancer metastasis: a potential role for heparinoids?

Schema {🗺️}

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