2012 Fiscal Year Final Research Report
Undifferentiated state induced by Rb inactivation associated with activation of inflammatory signaling
Project/Area Number |
23701048
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Tumor biology
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Research Institution | Kanazawa University |
Principal Investigator |
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Project Period (FY) |
2011 – 2012
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Keywords | Rb / p53 / Cancer stem cell / Inflammation |
Research Abstract |
Inactivation of Rb is frequently found during tumor progression. We found that Rb inactivation in p53 null background contributes to the acquisition of cancer stemness. RNA sequence analysis revealed that these cells exhibited signatures of inflammatory conditions. Knockdown experiments showed that sphere-forming activity induced by Rb depletion depend on activation of IL6 -STAT3 axis. Moreover, it seems that activation of STAT3 pathway induced by Rb inactivation directly cause an inflammatory tumor environment. These results are expected to provide some new insights into cell autonomous and non-cell autonomous function of Rb during tumor progression.
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