TY - JOUR
T1 - Perspectives on c-myc, cyclin D1, and their interaction in cancer formation, progression, and response to chemotherapy
AU - Liao, Dezhong J
AU - Thakur, Archana
AU - Wu, Jack
AU - Biliran, Hector
AU - Sarkar, Fazlul H.
PY - 2007
Y1 - 2007
N2 - C-myc is an oncogene that functions both in the stimulation of cell proliferation and in and apoptosis. C-myc elicits its oncogenic activity by causing immortalization, and to a lesser extent the transformation of cells, in addition to several other mechanisms. C-myc may also enhance or reduce the sensitivity of cancer cells to chemotherapy, but how this dual function is controlled is largely unclear. Cyclin D1 (D1) is another oncogene that drives cell cycle progression; it acts as a growth factor sensor to integrate extracellular signals with the cell cycle machinery, though it may also promote apoptosis. C-Myc collaborates with TGFα, epidermal growth factor receptor, Ras, PI3K/Akt, and NF-κB. in part via coordination in regulation of D1 expression, because D1 is a common downstream effector of these growth pathways. Coordination of c-Myc with D1 or its upstream activators not only accelerates tumor formation, but also may drive tumor progression to a more aggressive phenotype. Because c-Myc may effect immortalization while D1 or its upstream activators elicit transformation, targeting c-myc and D1 may be a good strategy for cancer prevention. Moreover, since D1 imposes chemoresistance on cancer cells, targeting D1 may also be a good strategy for cancer chemotherapy, whereas practicioners should be cautious to downregulate c-myc for chemotherapy, since c-Myc may elicit apoptosis.
AB - C-myc is an oncogene that functions both in the stimulation of cell proliferation and in and apoptosis. C-myc elicits its oncogenic activity by causing immortalization, and to a lesser extent the transformation of cells, in addition to several other mechanisms. C-myc may also enhance or reduce the sensitivity of cancer cells to chemotherapy, but how this dual function is controlled is largely unclear. Cyclin D1 (D1) is another oncogene that drives cell cycle progression; it acts as a growth factor sensor to integrate extracellular signals with the cell cycle machinery, though it may also promote apoptosis. C-Myc collaborates with TGFα, epidermal growth factor receptor, Ras, PI3K/Akt, and NF-κB. in part via coordination in regulation of D1 expression, because D1 is a common downstream effector of these growth pathways. Coordination of c-Myc with D1 or its upstream activators not only accelerates tumor formation, but also may drive tumor progression to a more aggressive phenotype. Because c-Myc may effect immortalization while D1 or its upstream activators elicit transformation, targeting c-myc and D1 may be a good strategy for cancer prevention. Moreover, since D1 imposes chemoresistance on cancer cells, targeting D1 may also be a good strategy for cancer chemotherapy, whereas practicioners should be cautious to downregulate c-myc for chemotherapy, since c-Myc may elicit apoptosis.
KW - C-myc
KW - Chemotherapy
KW - Cyclin D1
KW - Immortalization
KW - Transformation
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U2 - 10.1615/CritRevOncog.v13.i2.10
DO - 10.1615/CritRevOncog.v13.i2.10
M3 - Review article
C2 - 18197790
AN - SCOPUS:37249073366
SN - 0893-9675
VL - 13
SP - 93
EP - 158
JO - Critical Reviews in Oncogenesis
JF - Critical Reviews in Oncogenesis
IS - 2
ER -