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Autocrine IGF1 Signaling Mediates Pancreatic Tumor Cell Dormancy in the Absence
of Oncogenic Drivers
#MMPMID28249168
Rajbhandari N
; Lin WC
; Wehde BL
; Triplett AA
; Wagner KU
Cell Rep
2017[Feb]; 18
(9
): 2243-2255
PMID28249168
show ga
Mutant KRAS and c-MYC are oncogenic drivers and rational therapeutic targets for
the treatment of pancreatic cancer. Although tumor growth and homeostasis are
largely dependent on these oncogenes, a few residual cancer cells are able to
survive the ablation of mutant KRAS and c-MYC. By performing a genome-wide gene
expression analysis of in vivo-derived bulk tumor cells and residual cancer cells
lacking the expression of mutant KRAS or c-MYC, we have identified an increase in
autocrine IGF1/AKT signaling as a common survival mechanism in dormant cancer
cells. The pharmacological inhibition of IGF-1R reduces residual disease burden
and cancer recurrence, suggesting that this molecular pathway is crucial for the
survival of cancer cells in the absence of the primary oncogenic drivers.
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