ABCG1 (ATP Binding Cassette Subfamily G Member 1)

In 3D co-cultured human spheroid models, the peptide decreased markers of resistance (ABCG1, BCL2, CXCR4), stemness (WNT1, CD44) and ECM remodeling (COL1A1, MMP2/9, LOX) and enhanced gemcitabine efficacy...These effects were attributed to reduced desmoplasia, vasculature compression and enhanced infiltration of cytotoxic T cells and apoptosis. This study presents a novel cyclic peptide inhibiting ITGA5-mediated tumor-stroma interaction and thereby reduce desmoplasia and resistance, ultimately enhancing chemotherapy efficacy in PDAC.

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.

UGT1A1*6 and ABCC2 -24C > T variants emerge as potential predictors of irinotecan-induced neutropenia, while UGT1A1*6 and SLCO1B1 521T > C may serve as markers of prolonged PFS in Thai patients. Validation through larger prospective studies is essential to confirm and refine these genetic associations.

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.

Our findings revealed a novel mechanism by which ECM stiffness regulated ferroptosis via the Integrin-Hippo-ABCG1 pathway in LUAD. Nanodrugs designed to target ABCG1 demonstrate significant potential for future LUAD therapy by resensitizing tumors to ferroptosis (Fig. 1).

CAF-derived GAS6 induces GC chemoresistance via the AXL/STAT3/ABCG1 pathway. 9im restores chemosensitivity by inhibiting AXL and ABCG1-mediated efflux. AXL inhibitors with chemotherapy may improve GC treatment.

These findings underscore the pivotal role of cholesterol metabolic reprogramming in DLBCL progression. CD36 and related metabolic markers represent promising therapeutic targets, opening novel avenues for the treatment of this malignancy.

Ultimately, R@MLP shifted macrophages to the anti-inflammatory state and attenuated the progression of atherosclerosis. R@MLP synergizes checkpoint inhibition and cholesterol efflux to boost pro-efferocytosis therapy and presents a novel anti-inflammatory therapeutic strategy for atherosclerosis management.

Additionally, the cholesterol metabolism, potentially mediated by ABCG1, is implicated in PIM1's regulatory effect on the Th1, Th17, and Treg imbalance. Our study provides novel insights into the inflammatory imbalance during sepsis, which could facilitate the development of therapeutic strategies aimed at modulating the immune-inflammatory cascade in this condition.

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.

These findings indicate that CSF lipoproteins from patients with AD demonstrate impaired cholesterol delivery to neurons. Our study highlights APOE4 as a critical contributor to abnormal neuronal cholesterol uptake in AD pathophysiology.

CircABCA1 plays a crucial role in promoting ccRCC progression by regulating cholesterol metabolism and facilitating M2 macrophage polarization, representing a potential therapeutic target for ccRCC treatment.