ABCG2
- Known as:
- ABCG2
- Catalog number:
- 000934A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCG2
Related genes to: ABCG2
- Gene:
- ABCG2 NIH gene
- Name:
- ATP binding cassette subfamily G member 2 (Junior blood group)
- Previous symbol:
- -
- Synonyms:
- EST157481, MXR, BCRP, ABCP, CD338
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2019-04-23
Related products to: ABCG2
Related articles to: ABCG2
- Eg5 (also known as kinesin family member 11, encoded by the KIF11 gene) is a promising mitotic target for cancer therapy, yet no Eg5 inhibitor has achieved FDA approval to date. Their limited clinical efficacy may be linked to multidrug resistance, potentially involving ATP-binding cassette (ABC) transporters. However, the extent and specificity of such interactions remain unclear. This study investigates the interaction of the clinically evaluated Eg5 inhibitor litronesib with major ABC transporters and its role in transporter-mediated resistance. Eg5 expression was analyzed using data from the TCGA and HPA datasets. High-throughput molecular docking was used to screen a panel of 25 representative Eg5 inhibitors against ABCB1, ABCC1, and ABCG2. Subsequent functional validation in paired parental and transporter-overexpressing cell lines involved cytotoxicity and reversal assays, a [H]-paclitaxel accumulation assay, ATPase activity measurements, Western blotting, and immunofluorescence analysis. Database analysis revealed that Eg5 is overexpressed in multiple cancers and correlates with poor prognosis. High-throughput docking identified litronesib as a potential ABCB1 interactor with a strong predicted binding energy (-10.3 kcal/mol), while showing minimal predicted binding and no functional interaction with ABCC1 and ABCG2 in the models tested. ABCB1 overexpression conferred robust resistance to litronesib, which was reversed by verapamil. Litronesib induced a higher fold resistance than the classical ABCB1 substrates paclitaxel and doxorubicin (P < 0.05), and failed to reverse ABCB1-mediated multidrug resistance at non-cytotoxic concentrations. Mechanistically, litronesib strongly stimulated ABCB1 ATPase activity (EC ∼0.38 μM), modestly upregulated ABCB1 protein expression in a time-dependent manner, and enhanced intracellular [H]-paclitaxel accumulation only at high concentrations, without altering ABCB1 subcellular localization. Litronesib exhibits pronounced ABCB1-mediated resistance, a finding that underscores the need for strategies such as patient stratification or structural optimization to enhance efficacy. These findings provide a crucial framework for the resistance-aware development of new Eg5 inhibitors and will inform their future clinical applications. - Source: PubMed
Publication date: 2026/08/14
Wang YongZhang BohanPatel HarshLi ZheshenChen Xuan-YuChen XiangXie YuhaoCheng YexiaziLan YanningBo LetaoYu JinmingHu ManChen Zhe-Sheng - A flavonoid compound known as tectochrysin (TEC), which is extracted from Alpinia Oxyphylla Miq, possesses anti-cancer properties across a range of cancer types. This study aims to investigate its role in reversing sorafenib (SR) resistance in hepatocellular carcinoma (HCC) and the underlying mechanism. SR-resistant HCC cells (Huh7 SR and HCCLM3 SR) were generated through long-term induction of parental cells with escalating doses of SR. Cell viability was evaluated by CCK-8 assays. Cell proliferation was assessed by colony formation assays. Flow cytometry analysis was used to analyze cell apoptosis and cell cycle. Transwell and wound healing assays were applied to detect cell invasion and migration, respectively. Immunofluorescence staining was used to detect ABCG2 expression and p-AKT nuclear translocation. Cellular thermal shift assay (CETSA) and drug affinity responsive target stability (DARTS) assay were performed to validate the binding of TEC to PI3K and ABCG2 protein. HCC cell-derived xenograft models were used to confirm the anti-cancer effects of TEC in vivo. Western blot analysis was employed to detect the levels of proteins related to apoptosis, epithelial-mesenchymal transition (EMT), and the PI3K/AKT/ABCG2 pathway in cells and tissues. TEC significantly augmented the sensitivity of SR-resistant HCC cell lines to SR, synergistically inhibiting cell proliferation and colony formation. Combination treatment with TEC and SR potently induced G1/S cell cycle arrest and promoted apoptosis, accompanied by regulation of Bcl-2, Bax, C-PARP, C-caspase-3. Furthermore, TEC combined with SR effectively suppressed cell migration, invasion, and EMT, upregulating E-cadherin while downregulating N-cadherin and Vimentin. Mechanistically, TEC combined with SR exerted inhibitory effects on the PI3K/AKT/ABCG2 signaling. Evidence for this includes reduced expression of ABCG2, p-AKT, and p-PI3K, compromised ABCG2 expression, and attenuated nuclear translocation of p-AKT. In vivo, TEC and SR synergistically inhibited the growth of xenograft tumors derived from SR-resistant cells and reduced the expression of Ki67, ABCG2, and PI3K/AKT pathway proteins. Our study illustrates that TEC alleviates SR-associated chemoresistance in HCC cells by restraining activation of the PI3K/AKT signaling and inhibiting ABCG2 expression. This finding identifies TEC as a potential candidate to tackle SR resistance in HCC. - Source: PubMed
Publication date: 2026/08/14
Hu HanqingZheng XinTian GuodongLu LingXing Rongchun - To examine factors affecting the apparent clearance (CL/F) of total methotrexate polyglutamates (MTX-PGs) in red blood cells (RBCs) in Japanese patients with rheumatoid arthritis (RA) using population pharmacokinetic analysis. - Source: PubMed
Publication date: 2026/08/13
Hakamata JunKaneko YukoShimizu MikikoTakeuchi TsutomuHashiguchi Masayuki - Cancer pain affects more than half of all oncology patients and represents one of the most challenging therapeutic problems in modern medicine. Despite the central role of opioids in cancer pain management-codified by the WHO analgesic ladder-the clinical response to these agents is highly variable between individuals. Pharmacogenomics promises to explain this heterogeneity by identifying functionally relevant genetic polymorphisms in genes encoding opioid receptors, metabolizing enzymes, and membrane transport proteins. However, after two decades of intensive research, clinical translation of genetic data into actionable prescribing strategies remains elusive. A narrative-critical review of the literature was conducted by searching PubMed, Scopus, and Web of Science databases from inception to March 2026, using the search terms "opioid," "pharmacogenomics," "pharmacogenetics," "cancer pain," "polymorphism," and individual gene names (OPRM1, CYP2D6, COMT, ABCB1, SLC22A1, UGT2B7, and others). Reference lists of included articles were hand-searched for additional relevant studies. Inclusion was restricted to English-language articles reporting original data or systematic reviews on genetic polymorphisms and opioid response, with priority given to studies conducted in cancer pain populations. Clinical practice guidelines from CPIC, NCCN, ESMO, EAPC, and ASCO were consulted for current recommendations. This narrative-critical review examines the evidence on genetic polymorphisms relevant to opioid response in cancer pain, covering three functional categories: (1) pharmacodynamic genes, including opioid receptors (OPRM1, OPRD1, OPRK1) and neuromodulatory targets (COMT, KCNJ6, MC1R); (2) pharmacokinetic enzymes (CYP2D6, CYP3A4/5, UGT2B7); and (3) membrane transporters, including ABC efflux pumps (ABCB1, ABCG2, ABCC2) and SLC uptake carriers (SLC22A1, SLCO1B1, SLC6A4, SLC6A2). A dedicated section addresses the direct and indirect interference of the tumour itself-through the tumour microenvironment, neuroimmune signalling, epigenetic reprogramming, and cancer-induced organ dysfunction-on opioid pharmacogenomics. The overall evidence is poor and fragmented, a finding intrinsic to the extraordinary diversity, large number, and context-dependent biological activity of the polymorphisms identified. The tumour itself acts as a pervasive confounder that systematically distorts genotype-phenotype relationships. The path forward requires a paradigm shift from candidate-gene association studies to system pharmacogenomics and multi-omic integration. - Source: PubMed
Publication date: 2026/08/04
Mercadante Sebastiano - Heat stress limits dairy production. The temperature-humidity index (THI), combining temperature and relative humidity, is widely used to assess heat stress. However, in Chinese Holstein cattle, the phenotypic responses of milk traits and genotype-environment interaction mechanisms under different THI conditions are understudied. Based on 63,334 records from 7240 cows (milk yield, fat percentage, protein percentage), matched with meteorological data and 113,297 SNPs, we employed a random-effects GWAS to examine SNP effects across a continuous THI gradient, comparing results with conventional, temperature-, and humidity-interaction GWAS. As THI increased, all traits declined with distinct patterns. Random regression GWAS identified 149 significant SNP × THI interactions (5 for MY, 86 for FP, 58 for PP), distributed across BTA5, BTA6, BTA14, and BTA20. Candidate gene annotation identified 52 candidate genes near significant SNPs, of which 50 core candidate genes were supported in both temperature and humidity GWAS. The most robustly supported core candidate genes include , , , , , , , , , and -of which , , and have been functionally validated in milk production traits, whereas others represent novel candidates requiring further investigation. Temperature and THI-GWAS showed high consistency, while humidity-GWAS detected both overlapping and specific signals. Incorporating THI as a continuous environmental gradient identifies environment-dependent regulatory signals not captured by conventional GWAS, providing candidate genes that may contribute to future breeding strategies after further validation. - Source: PubMed
Publication date: 2026/08/03
Ou KangliZheng KunTeng JunLi YanZhang QinNing ChaoWang Dan