ABCB6 (ATP Binding Cassette Subfamily B Member 6 (Langereis Blood Group))

This study established and validated a prognostic model for HCC by using CRGs and demonstrated high predictive effectiveness. These findings enhance the understanding of CRGs and offer theoretical support for prognostic prediction in HCC.

To explore the impact of erythroid differentiation on CP levels, we treated K562 cells with imatinib to induce Hb synthesis...This study addressed the question of how CPs are released from the red blood cells and found that active transport mechanisms, especially mediated by MRP4, ABCB6, and breast cancer resistance protein are likely involved in the efflux of CPs from erythroid cells. This suggests the reduced function of these efflux transporters may affect plasma CP levels.

The MRGs-high subgroup showed heightened sensitivity to cisplatin but resistance to erlotinib, and impaired immunotherapy responses, which has potential clinical transformation value in the design of individualized combination therapy. Functional validation revealed ABCB6 as a key oncogenic driver, with genetic depletion significantly attenuating HCC cell proliferation, migration, and invasion in vitro. Collectively, the MRGs signature serves as a better predictor of HCC prognosis and therapeutic resistance, while its core component ABCB6 emerges as a critical regulator of HCC malignancy.

This unique dual role of SASH1 highlights its importance in melanocyte homeostasis and UV-induced pigmentation. Understanding the role of SASH1 in regulating pigmentation can help foster novel therapeutic approaches for these genodermatoses and related pigmentary anomalies, ultimately improving patient care and outcomes.

The findings evidenced that the SALL4/ABCB6 axis suppresses mitophagy to hinder ferroptosis in CC. The mitophagy pathway may be essential for ABCB6 to regulate ferroptosis in CC.

Ultimately, the immune microenvironment and enrichment pathways were analyzed among individuals categorized as high-risk and low-risk. The predictable ion homeostasis-associated 15 gene signature established in this study predicts overall survival outcomes in patients with KIRC, to some extent helping clinicians to select personalized treatment regimens.

After partial purification and in the presence of the detergent (n-dodecyl-β-D-maltoside), the kinetic parameters of the ATP hydrolysis reactions of the orthologs were determined, as well as the extent of stimulation of their activity when presented with putative substrates. We discuss the efficiency of such bioinformatics approaches and make suggestions for their improvement and wider application in membrane protein-structure determination.

Inhibiting TRIM9 caused a decrease in the IC50 of doxorubicin (DOX), and significant increases in the intracellular uptake, retention and absorption of DOX in HepG2/ADR cells. These findings may provide new insights into the mechanism of MDR development. The MDR-related hub genes, especially TRIM9 may be targeted therapeutically to enhance the prognosis of patients with drug-resistant HCC.

We delve into the molecular pathways of ferroptosis, highlighting the involvement of NFE2L2 and its target genes, such as NQO1, HMOX1, FTH1, FTL, HERC2, SLC40A1, ABCB6, FECH, PIR, MT1G, SLC7A11, GCL, GSS, GSR, GPX4, AIFM2, MGST1, ALDH1A1, ALDH3A1, and G6PD, in ferroptosis resistance. Understanding the delicate balance between NFE2L2's protective and deleterious roles could pave the way for novel therapeutic strategies targeting NFE2L2 to enhance the efficacy of ferroptosis inducers in cancer therapy.

The outcomes of this study contribute to a comprehensive understanding of the implications of ABCB family genes in tumor progression, offering insights into potential therapeutic targets for cancer. Notably, the identification of ABCB6 as a significant oncogene suggests promising avenues for targeted therapies in KIRP, LIHC, and PAAD.

In this review, we summarize current knowledge concerning transport of Cd and its complexes (mainly Cd bound to glutathione) by the ABC transporters ABCB1 (P-glycoprotein, MDR1), ABCB6, ABCC1 (multidrug resistance related protein 1, MRP1), ABCC7 (cystic fibrosis transmembrane regulator, CFTR), and ABCG2 (breast cancer related protein, BCRP). Potential detoxification strategies underlying ABC transporter-mediated efflux of Cd and Cd complexes are discussed.

ABC transporters, especially ABCC1 seem to contribute substantially to AML chemoresistance. A detailed understanding of chemoresistance mechanisms and the clinical implications of chemosensitivity predictors may lead to alternative therapeutic approaches for AML patients with unveiled chemoresistance signatures.