Recent Phase II clinical trial data studying entinostat and azacitidine in metastatic breast cancer revealed that induction of several pro-dormancy genes post-treatment was associated with prolonged patient survival. Together, these findings suggest HDACi as a potential therapeutic avenue to promote dormancy, prevent recurrence, and improve patient outcomes in breast cancer.
These results indicate that the LIFR/STAT3 pathway may mediate either tumor promoting or tumor suppressive signaling pathways depending on the genetic background of tumor cells, and may play diverse roles within other cells in the tumor microenvironment. Implications: Mutant KRAS drives downregulation of the receptor for leukemia inhibitory factor, thereby allowing an increase in expression of the glucose transporter GLUT1 and increases in glycolysis and mitochondrial respiration.
Our data allow us to conclude that ILEI participates in the regulation of LIFR gene transcription, which plays a role in ILEI-induced maintenance of spheroid formation and self-renewal. Continued investigation will allow development of studies aimed at revealing the mechanisms involved in ILEI/LIFR axis-mediated disease progression in vivo.
circ_0001073 increased LIFR expression via miR-626 in lung cancer cells. In conclusion, circ_0001073 represses lung cancer progression via miR-626/LIFR axis, indicating the potential value of circ_0001073 in lung cancer treatment.
LIF was up-regulated and high LIF expression was associated with poor prognosis while LIFR was down-regulated and high LIFR expression was associated with favorable prognosis in pancreatic adenocarcinoma. LIF and LIFR might be therapeutic targets and prognostic markers for individual therapy of pancreatic adenocarcinoma.
12 months ago
KRAS (KRAS proto-oncogene GTPase) • STAT3 (Signal Transducer And Activator Of Transcription 3) • LIFR (LIF Receptor Subunit Alpha)
Eight cohorts containing 1278 cases with PAAD were identified and the analysis results suggested that LIF was highly expressed while LIFR was lowly expressed in PAAD tissues compared with adjacent or normal tissues. Kaplan-Meier plot curves and univariate and multivariate Cox proportional hazards regression analyses indicated high LIF expression was associated with shorter overall survival (adjusted hazard ratio = 1.641, 95% CI: 1.399-1.925, p < 0.001) whereas high LIFR expression was associated with longer overall survival (adjusted hazard ratio = 0.653, 95% CI: 0.517-0.826, p < 0.001).
High LIF/LIFR levels indicated shorter biochemical recurrence-free survival among patients who underwent radical prostatectomy. Therefore, the lncAMPC/LIF/LIFR axis plays a critical role in PCa metastasis and immunosuppression and may serve as a prognostic biomarker and potential therapeutic target.
These results demonstrated that low LIFR expression reduces the neuroprotective efficacy of LIF in aged rodents of both sexes. Furthermore, the ability of LIF to promote motor improvement is dependent upon sex in aged rodents.