TY - JOUR
T1 - Direct activation of Bmi1 by twist1
T2 - Implications in cancer stemness, epithelial-mesenchymal transition, and clinical significance
AU - Wu, Kou Juey
PY - 2011/5
Y1 - 2011/5
N2 - Cancer stemness is a concept used to describe a minor population of cells (cancer stem cells-CSCs) residing in a tumor, which possess self-renewal properties and are resistant to chemo/radiation therapy. Epithelial-mesenchymal transition (EMT), a major mechanism of cancer metastasis, is a process which generates cells with stem-like properties. The relationship between cancer stemness and EMT is well documented but without detailed mechanistic explanation. Bmi1 belongs to the polycomb repressive complex 1 (PRC1) which maintains self-renewal and stemness. Recent results showed that Twist1, an EMT regulator, directly activates Bmi1 and these two molecules function together to mediate cancer stemness and EMT. These results provide a molecular explanation of the relationship between cancer stemness and EMT. Bmi1 is frequently overexpressed in various types of human cancers and can confer drug resistance. Twist1 is also overexpressed in various human cancers with prognostic significance. The functional interdependence between Twist1 and Bmi1 provides a fresh insight into the molecular mechanism of EMT-induced cancer stemness. Further investigation of the mechanisms mediating EMT and cancer stemness will be helpful in the management and treatment of metastatic cancers.
AB - Cancer stemness is a concept used to describe a minor population of cells (cancer stem cells-CSCs) residing in a tumor, which possess self-renewal properties and are resistant to chemo/radiation therapy. Epithelial-mesenchymal transition (EMT), a major mechanism of cancer metastasis, is a process which generates cells with stem-like properties. The relationship between cancer stemness and EMT is well documented but without detailed mechanistic explanation. Bmi1 belongs to the polycomb repressive complex 1 (PRC1) which maintains self-renewal and stemness. Recent results showed that Twist1, an EMT regulator, directly activates Bmi1 and these two molecules function together to mediate cancer stemness and EMT. These results provide a molecular explanation of the relationship between cancer stemness and EMT. Bmi1 is frequently overexpressed in various types of human cancers and can confer drug resistance. Twist1 is also overexpressed in various human cancers with prognostic significance. The functional interdependence between Twist1 and Bmi1 provides a fresh insight into the molecular mechanism of EMT-induced cancer stemness. Further investigation of the mechanisms mediating EMT and cancer stemness will be helpful in the management and treatment of metastatic cancers.
KW - Bmi1
KW - Cancer stemness
KW - Epithelial-mesenchymal transition
KW - Twist1
UR - http://www.scopus.com/inward/record.url?scp=79959972120&partnerID=8YFLogxK
M3 - 文献综述
C2 - 21733352
AN - SCOPUS:79959972120
SN - 0255-8270
VL - 34
SP - 229
EP - 238
JO - Chang Gung Medical Journal
JF - Chang Gung Medical Journal
IS - 3
ER -