Fig. 1

Oncogenic KRAS regulates the expression of LIF, but not other IL-6 family cytokines. a Representative western blots showing the amounts of LIF, KRAS, and phosphorylated STAT3 at Y-705 in multiple human and mouse pancreatic cancer cell lines where wild-type or mutant KRAS have been stably knocked down by shRNAs. b Representative western blots showing increased expression of LIF, KRAS, and phosphorylated STAT3 at Y-705 in mouse pancreatic adenocarcinoma cell line (iKRAS*). Representative qPCR showing increased mRNA expression of LIF and KRAS in the same cell line (N = 3; **P < 0.01; ****P < 0.0001). Error bar represents the standard deviation and P-value was generated by t-test. Its expression of KRAS was reactivated by adding 1 µg/mL of doxycycline in growth medium. iKRAS* line was harvested and established from pancreatic tumor developed in a p48Cre; TetO-KrasG12D; Rosa26rtTa/+; p53R172H/+mouse. c Western bot suggesting increased expression of LIF in KRAS mutant human pancreatic cancer cell lines, Panc1.0 and Panc2.03, which had higher RasGTP level when compared to KRAS wild-type cell line, BxPC3. RasRBD pull-down assay was used to determine RasGTP level. The cells were serum-starved for 24 h before harvested for RasRBD pull-down. d Oncomine analysis suggesting upregulation of human LIF, but not IL-6, in the human cancer cell lines where KRAS is mutant when compared with cells expressing wild-type KRAS.The analysis in the pan-cancer cell lines (KRAS WT vs mutant) (Nature volume 483, pages 570–575 (29 March 2012)) was performed by using Oncomine Platform Software (Invitrogen; https://www.oncomine.org/resource/login.html)