LPCAT1 (Lysophosphatidylcholine Acyltransferase 1)

Notably, the AXL inhibitor Bemcentinib effectively suppressed CML-BP progression in both in vivo and in vitro models. Collectively, our findings establish SE-driven SOX4 and SMAD3 as key regulators in CML-BP and identify Bemcentinib as a promising therapeutic strategy.

LPCAT1 upregulates cell cycle proteins through activation of the PI3K/AKT signaling pathway, thereby promoting cellular proliferation and accelerating ICC progression.

Its overexpression in HCC cells potently enhanced proliferation, migration, and invasion. LPCAT1 is a vital prognostic biomarker and putative therapeutic target in HCC.

In vitro experiments further showed that DEHP and MEHP promote the proliferation and migration of breast cancer cells (MCF-7 and MDA-MB-231), enhance lipid accumulation and mitochondrial function, and validate the altered expression of these prognostic genes at the transcriptional level, with MEHP exerting more pronounced effects. In conclusion, this study suggests that DEHP and MEHP may activate metabolic reprogramming in breast cancer, thereby contributing to disease progression and poorer prognosis, highlighting these genes as potential prognostic biomarkers and therapeutic targets.

Our 9-LRG panel is a promising classifier for assessing the prognosis of BRCA. Notably, targeting EIF4EBP1 could potentially serve as a theoretical foundation for enhancing the prognosis of BRCA patients.

CONCLUSIONS Our findings suggest multi-omic switch-like regulation may underlie differential COPD/IPF etiology. Future investigation of LPCAT1 and ATP11A could provide new mechanistic understanding and therapeutic avenues.

In vivo, LPCAT1 enhanced tumor growth, lung metastasis, and cholesterol metabolism, while these effects were counteracted by SOX2 inhibition. The SOX2/LPCAT1 axis drives osteosarcoma progression by modulating cholesterol metabolism.

Analysis of public LUSC data confirmed associations between the expression levels of genes encoding enzymes involved in the biosynthesis pathways of arginine, proline (ASL, OTC, PYCR2), PC (CEPT1, CHPT1, LPCAT1) and LPC (LCAT, PLA2G16, PLB1) with a 5-yr survival outcome. The observed metabolic reprogramming in LUSC patients suggested the potential utility of metabolites as a supportive biomarkers for LUSC diagnosis.

Our findings suggest that scFv-MML@LPCAT1si represents a promising targeted therapy for NSCLC BM, leveraging the unique properties of scFv-MML to traverse the BBB and deliver therapeutic payloads to tumor sites with high accuracy and efficiency.

This study provides a comprehensive framework for understanding sorafenib resistance in HCC, alongside a validated prognostic model that holds potential for clinical application.

This study provides the first comprehensive analysis of LDAGs in EC, establishing robust prognostic and diagnostic gene signatures with strong biological relevance. These signatures support a metabolism-driven framework for EC classification and may offer potential clinical utility in early detection, risk stratification, and personalized treatment.

Moreover, a novel prognostic prediction nomogram was also developed, which possessed excellent prognostic prediction capabilities. We hope the novel LRG-related subtypes and nomogram of HCC would provide new insights and guidelines for clinical practice in the future.