2014
DOI: 10.1016/j.dnarep.2014.07.001
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Akt and p53R2, partners that dictate the progression and invasiveness of cancer

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Cited by 44 publications
(26 citation statements)
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“…In case of certain other anticancer drugs, SLC7A11 suppresses the expression of the proteins that are targets for the drugs. For example, gemcitabine in the form of its diphosphate produces its anticancer effects by inhibiting ribonucleotide reductase; SLC7A11 reverses this effect by directly activating the enzyme with glutathione or inducing the expression of the enzyme with glutathione-dependent activation of p53 (35,36). Therefore, pharmacologic blockade of the transport function of SLC7A11 not only interferes with tumor growth but also reverses resistance to certain chemotherapeutic agents.…”
Section: Slc7a11 and Its Functional Coupling To Slc1a5 In Cancer: Relmentioning
confidence: 99%
“…In case of certain other anticancer drugs, SLC7A11 suppresses the expression of the proteins that are targets for the drugs. For example, gemcitabine in the form of its diphosphate produces its anticancer effects by inhibiting ribonucleotide reductase; SLC7A11 reverses this effect by directly activating the enzyme with glutathione or inducing the expression of the enzyme with glutathione-dependent activation of p53 (35,36). Therefore, pharmacologic blockade of the transport function of SLC7A11 not only interferes with tumor growth but also reverses resistance to certain chemotherapeutic agents.…”
Section: Slc7a11 and Its Functional Coupling To Slc1a5 In Cancer: Relmentioning
confidence: 99%
“…[43,44] AMPK is the key enzyme that regulates glucose homeostasis, lipid metabolism, and insulin sensitivity. [49,52,53] Similarly, metformin treatment has been proved to have chemo-preventive effects in ovarian cancer cells. [45] 2-Indirect activation occurs when upstream kinases such as liver kinase B1 (LKB-1) phosphorylates the catalytic domain of AMPK ( Figure 2).…”
Section: Biguanidesmentioning
confidence: 99%
“…CAF‐expressed proteins are main links of CAFs with MDR (Figure ). Accumulating studies have shown that HGF signaling is involved in the progression of MDR by activating both MAPK and PI3K‐AKT signaling pathways and consequently inhibiting the drug‐induced apoptosis . Therefore, HGF signaling confers MDR via upregulation of AKT and MAPK signaling pathways.…”
Section: Resistance To Therapies Mediated By Breast Tumor Stromamentioning
confidence: 99%