PMC:4307189 / 51621-52559 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4307189","sourcedb":"PMC","sourceid":"4307189","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4307189","text":"Komurov et al. [17] hypothesized that cross-talks between EGFR/ErbB signaling and metabolic pathways contribute to resistance to lapatinib. More specifically, they identified that glucose deprivation reduces the inhibiting effects of lapatinib by up-regulating constituent genes and thus providing an EGFR/ErbB2-independent mechanism of glucose uptake and cell survival [17]. Here, by using the same gene expression datasets, we found MDM2:STK11 cross-talk between EGFR/ErbB and IGF1R signaling, where STK11 (also known as LKB1) phosphorylates and activates AMPK in absence of glucose [67]. Again, in the integrated signaling circuitry of pathways: p53-IGF-1-AKT-TSC2-mTOR, a positive feedback loop (p53-PTEN AKT-MDM2-p53) is formed which enhances p53-mediated apoptosis and senses nutrient deprivation [67]. Thus our results complement the findings of Komurov et al. by finding signaling cross-talks between EGFR/ErbB and IGF1R pathways.","tracks":[{"project":"2_test","denotations":[{"id":"25599599-16452501-14868176","span":{"begin":586,"end":588},"obj":"16452501"},{"id":"25599599-16452501-14868177","span":{"begin":804,"end":806},"obj":"16452501"}],"attributes":[{"subj":"25599599-16452501-14868176","pred":"source","obj":"2_test"},{"subj":"25599599-16452501-14868177","pred":"source","obj":"2_test"}]}],"config":{"attribute types":[{"pred":"source","value type":"selection","values":[{"id":"2_test","color":"#ecb093","default":true}]}]}}