2022
DOI: 10.1007/978-3-030-94004-1_10
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KRAS Addiction Promotes Cancer Cell Adaptation in Harsh Microenvironment Through Macropinocytosis

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Cited by 1 publication
(2 citation statements)
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“…99 After PI3K activation, mTOR is subsequently activated in cells. 100 In particular, KRAS can directly bind to PIK3CA to activate the PI3K pathway, which causes the activation of mTOR. In addition, the loss of function of tumor suppressor proteins such as PTEN, p53, and TSC1/TSC2 will lead to the activation of mTOR in the pathological state of tumors.…”
Section: ■ Polysaccharides and Cancersmentioning
confidence: 99%
See 1 more Smart Citation
“…99 After PI3K activation, mTOR is subsequently activated in cells. 100 In particular, KRAS can directly bind to PIK3CA to activate the PI3K pathway, which causes the activation of mTOR. In addition, the loss of function of tumor suppressor proteins such as PTEN, p53, and TSC1/TSC2 will lead to the activation of mTOR in the pathological state of tumors.…”
Section: ■ Polysaccharides and Cancersmentioning
confidence: 99%
“…PIK3CA mutations induce sustained activation of the mTOR/PI3K/AKT pathway, which reduces cell dependence on growth factors and stimulates cell growth and conversion . After PI3K activation, mTOR is subsequently activated in cells . In particular, KRAS can directly bind to PIK3CA to activate the PI3K pathway, which causes the activation of mTOR.…”
Section: Mtor and Cancersmentioning
confidence: 99%