ABCA1 (ATP Binding Cassette Subfamily A Member 1)

The activation of THP-1 cells induced by MPO protein directly impaired in vitro microvascular structure via increasing the expression of IL-6 and TNFα regulated by NF-κB p65 of THP-1 cells. Together, the noncatalytic functions entail MPO and PON in modulating the involvement of monocytes and endothelial cells in atherosclerosis.

Mechanistically, it blocks the LXR/Abca1 axis, reducing myelin lipid transfer from lipid-laden macrophages (LLMs) and downregulating T cell KLRB1, thereby augmenting T cell activation and antitumor activity. cEV@GSK enhances T cell immunity by disrupting the LXR/Abca1 axis and LLM-mediated lipid transfer, offering a novel GBM immunotherapy strategy.

The clarification and materials provided by the authors upon request did not address the concerns. Accordingly, the article is retracted as the editors have lost confidence in the integrity and accuracy of the whole body of data presented in the article and consider its conclusions invalid.

Early-stage HCC induces a reversible, systemic immunosuppressive transcriptome captured by a monocyte-derived 23-gene blood signature; tumor removal partially restores this profile within three months. These results highlight the potential of blood-derived monocyte signatures as noninvasive biomarkers of HCC-associated immunosuppression and clinical outcome.

We conclude that SKLB06489 is a potent type Ⅰ PRMTs inhibitor with great therapeutic potential and is expected to overcome the TNBC treatment bottleneck. The discovery of SKLB06489-regulated cholesterol homeostasis provides a novel perspective on the biological function of type Ⅰ PRMTs, particularly their role in regulating metabolic pathway.

An antisense oligonucleotide targeting rs737540 significantly inhibited OSCC proliferation and reversed membrane cholesterol-induced resistance. This study provides novel insights into how genetic variants regulating alternative splicing contribute to OSCC risk and identifies potential therapeutic targets.

Inhibiting esterification of cholesterol, which renders it inert, selectively suppresses growth of a xenograft model of Snail-positive kidney cancer. Our findings offer a new perspective on lipid-targeting strategies for invasive cancer therapy.

Restoring cholesterol balance through LXR agonists, cyclodextrins, or strategies that enhance ABCA1 function holds promise for limiting renal toxicity while simultaneously impairing tumor survival mechanisms. Advances in lipidomics, metabolic imaging, and biomarker-driven stratification may facilitate precision approaches that integrate metabolic correction with effective oncologic care.

Meta-analyses of clinical data reveal that neonatal hyperbilirubinemia (jaundice) caused by high levels of bilirubin, increases pediatric brain tumor risk. Collectively, these findings highlight the origins of sex differences in neurodevelopment and brain tumorigenesis, offering insights into early screening and prevention of pediatric brain tumors through targeted interventions addressing modifiable risk factors.

Tumors grown in these mice were also more resistant to immune therapy. Therefore, modulating ABCA1 activity within MCs may represent a previously unidentified approach to immune therapy.

This multi-omics, public data-driven synthesis delineates a coherent network of genomic, epigenomic, transcriptomic, and structural vulnerabilities, offering a rational framework for therapeutic targeting of cholangiocarcinoma. This study reveals novel bile duct-associated variations that expand our understanding of cholangiocarcinoma pathogenesis and provide potential targets for precision medicine approaches.

Also, administration of 2, 4-DTBP improved the neuropathies and locomotor function recovery after SCI.Taken together, activation of RXRα decreased the formation of FMMs by promoting cholesterol efflux and inhibited neuroinflammation by inhibition of p38 and NF-κB signaling after SCI. It is a promising target for mitigating FMMs-induced neuroinflammation and locomotor dysfunction.