LIFR (LIF Receptor Subunit Alpha)

Transcriptional (Twist1/NR2F2) and post-transcriptional (miRNA-mediated) regulatory mechanisms were implicated in LIFR-driven pathogenesis. Our study first investigated NF-serum proteomic concordance as a predictor of PR and demonstrated the potential of integrated multi-compartment analysis for predicting recurrence.

The pharmacokinetics study strengthened our results that the identified drugs can be used as a therapeutic for PDAC as they obey Lipinski's rule. In conclusion, identified genes can act as prognostic markers, and drugs could be used as potential therapeutics for PDAC.

This study established causal relationships between specific immune cell phenotypes, inflammatory cytokines, and AA. Importantly, LIF partially mediated the effects of immune cells on AA, suggesting the LIF-LIFR axis as a potential therapeutic target.

Exposure of PDCA cell lines to LRI310 suppresses STAT3 activation and counteracts effects of LIF on proliferation and CAF-inducing transcriptional programs. Collectively, these findings identify LIF as an important epithelial driver of CAF-oriented transcriptional programs in PDAC and support the development of LIFR antagonism as a promising strategy to modulate the desmoplastic microenvironment.

LIF/LIFR protein accumulated from 2-72 h (48 h apex). These time-resolved data reveal progressive oedema with sustained oxidative burden and a LIF-JAK1-STAT3 activation peak, suggesting a therapeutic window in AHH-induced retinal injury.

SWS is a rare autosomal recessive disorder characterized by autonomic dysfunction and bent-bone dysplasia due to pathogenic homozygous or compound heterozygous variants in the LIFR gene. Management is currently supportive, and further research is required to improve treatment and prognosis.

Functional assays demonstrated that GHR overexpression suppressed proliferation, migration, and invasion while promoting apoptosis. Our study integrates bulk and single-cell transcriptomics with functional validation, unveiling cytokine-driven mechanisms in HBV-HCC. The cytokine-based prognostic model holds promise for risk stratification, immunomodulation, and personalized therapy, offering new avenues for improving HBV-HCC management.

IL-13 and LIFR affect the blood concentrations of 6 metabolites, and 3 metabolites influence IL-13 or LIFR levels, no evidence supports these metabolites acting as intermediaries in regulating AA risk. This study identifies inflammatory cytokines and blood metabolites as potential pathogenic factors in AA.

Collectively, these data define a molecular continuum from chronic gastritis to GC and highlight LIFR, IL10RB, SERPINE1 and HGF as pivotal biological macromolecules and candidate therapeutic targets. The repurposing potential of anti-inflammatory agents, particularly rofecoxib and nabumetone, suggests a feasible strategy to intercept the gastritis-carcinoma sequence.

Our findings indicate that BC can target LIFR in hCMEC/D3 cells via exosomal miR-221-3p, thereby promoting glycolysis and inhibiting the expression of tight junction proteins, which facilitates tumor metastasis.

This study demonstrates a causal relationship between circulating inflammatory proteins and cervical cancer risk in both European and Asian populations. The findings highlight both pro-cancer and protective roles of specific inflammatory proteins, offering insights for biomarkers in cervical cancer risk assessment and prevention strategies.

Early identification of the LIFR gene variant is crucial for timely intervention and management of multi-system complications. Further research is warranted to explore targeted therapies and improve outcomes for patients with this rare disorder.