ABCC9
- Known as:
- ABCC9
- Catalog number:
- 000916A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCC9
Related genes to: ABCC9
- Gene:
- ABCC9 NIH gene
- Name:
- ATP binding cassette subfamily C member 9
- Previous symbol:
- -
- Synonyms:
- SUR2, CMD1O
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2019-04-23
Related products to: ABCC9
Related articles to: ABCC9
- Gastrointestinal (GI) cancers remain a leading cause of cancer-related mortality worldwide, with limited therapeutic options for advanced disease due to tumor heterogeneity, metastasis, cancer stemness, and acquired drug resistance. Cyclin-dependent kinases 7 and 9 (CDK7/9) are key regulators of transcription and cell-cycle progression, and their aberrant activation sustains oncogenic transcriptional programs. GNE-3511 is a dual CDK7/9 inhibitor with favorable pharmacokinetics, making it a promising therapeutic candidate for cancer treatment. The aim of the study is to investigate the anticancer efficacy and molecular mechanisms of GNE-3511 in gastrointestinal cancer models. Anticancer activity was evaluated in colorectal (HCT116), hepatocellular (HepG2), gastric (NCI-N87), and pancreatic (PanC1) cancer cells using cell viability, cell-cycle, apoptosis, migration, sphere formation, cancer stem cell, and doxorubicin accumulation assays. Expression of genes and proteins associated with apoptosis, epithelial-mesenchymal transition (EMT), stemness, multidrug resistance, and CDK7/9 signaling was analyzed by RT-qPCR and immunoblotting. Therapeutic efficacy was validated in an HCT116 xenograft model, with molecular analyses confirming the underlying anticancer mechanisms. GNE-3511 treatment reduced cell viability in all GI cancer cell lines, with the greatest potency in HepG2 followed by HCT116 cells. Further, GNE-3511 treatment induced G1 or G2/M cell-cycle arrest and promoted apoptosis by increasing BAX expression and suppressing BCL2, MCL1, and Survivin. GNE-3511 significantly reduced CD133⁺ and CD90⁺ cancer stem cell populations, inhibited migration, spheroid formation, and downregulated the stemness- and EMT-associated regulators Nanog, Snail, Twist, Vimentin, and Zeb1. Moreover, GNE-3511 enhanced intracellular accumulation of doxorubicin by repressing the multidrug resistance transporters ABCB1, ABCC9, and ABCG2. In HCT116 xenografts, GNE-3511 markedly suppressed tumor growth while reproducing the molecular effects observed in vitro. Furthermore, GNE-3511 did not cause treatment-related abnormalities, indicating favorable safety. Mechanistically, GNE-3511 inhibited CDK7/9 signaling, resulting in RB hypophosphorylation, suppression of POLR2A, and depletion of the oncogenic transcriptional regulators cMyc and MCL1. GNE-3511 exerts potent anticancer activity by disrupting CDK7/9-dependent transcriptional programs that regulate proliferation, apoptosis, stemness, EMT, and multidrug resistance. These findings identify GNE-3511 as a potential lead candidate for the treatment of colorectal cancers. - Source: PubMed
Publication date: 2026/08/21
Sharma NidhiPanneerselvam SuriyaBharate Sandip BAndugulapati Sai Balaji - Cantú syndrome (CS) comprises a group of rare multisystem and multi-organ diseases characterized by congenital hypertrichosis, facial dysmorphism, cardiomegaly, and skeletal abnormalities, as well as other clinical manifestations. The current understanding of CS is limited. It is easy to misdiagnose it due to its diverse clinical manifestations and a lack of awareness of the condition. Currently, it is thought that this disorder is inherited in an autosomal dominant manner and caused by mutations in the ATP-sensitive potassium (K) channel, which plays a vital role in both cardiovascular diseases and diabetes. There are currently no effective or specific treatments for CS, and there is a lack of research on the mechanisms of and therapy for this disease. Therefore, it is essential to raise awareness and educate people on CS. Herein, we summarize reported knowledge about CS, including its epidemiology, definition, clinical features, diagnosis, and treatment. - Source: PubMed
Publication date: 2026/07/16
He ShuijingHu DanNichols Colin GHuang Yan - : Cantú syndrome (OMIM #239850) is a rare autosomal dominant disorder caused by gain-of-function variants in or , which encode subunits of the ATP-sensitive potassium (K) channel. Its characteristic features-generalized hypertrichosis, coarse facial appearance, skeletal abnormalities, and cardiovascular involvement-may be overlooked when other major comorbidities dominate the clinical picture. : A 29-year-old Taiwanese woman, born prematurely and complicated by neonatal hydrocephalus with subdural hemorrhage requiring ventriculoperitoneal shunt placement, had been followed since infancy under a working diagnosis of cerebral palsy with left hemiparesis and borderline-to-mild intellectual disability. Over the ensuing years, additional features gradually emerged, including generalized hypertrichosis with thick scalp and body hair, coarse facial features, bilateral hallux valgus, mild thoracic scoliosis, polycystic ovaries, mild aortic regurgitation, recurrent hemoptysis associated with abnormal pulmonary vasculature, and iron-deficiency anemia. Earlier genetic investigations-including chromosome analysis (46,XX), array comparative genomic hybridization (array-CGH; 2013), and a trio-based next-generation sequencing study performed under a national rare disease research initiative (2019)-were unrevealing. Whole-genome sequencing performed in December 2025 identified a heterozygous variant (NM_020297.4:c.4174A>G, p.(Ile1392Val)), initially classified as a variant of uncertain significance. Parental Sanger sequencing confirmed the variant to be de novo, and reclassification according to ACMG/AMP criteria supported a likely pathogenic interpretation. Re-evaluation of the patient's phenotype demonstrated findings consistent with Cantú syndrome. : This case illustrates how Cantú syndrome may remain unrecognized for years when a prominent neurological comorbidity-perinatally acquired hydrocephalus and presumed cerebral palsy-dominates the clinical narrative. We report a previously undescribed de novo missense variant (c.4174A>G, p.(Ile1392Val)), thereby expanding the mutational spectrum associated with Cantú syndrome. This case also highlights the practical value of resequencing and periodic reanalysis using updated next-generation sequencing platforms in patients with long-standing undiagnosed disease, even after prior negative genetic testing. - Source: PubMed
Publication date: 2026/07/15
Lee Chung-LinChang Ya-HuiChuang Chih-KuangChiu Huei-ChingTu Yuan-RongLo Yun-TingWu Jun-YiLin Hsiang-YuLin Shuan-Pei - - Source: PubMed
Publication date: 2026/07/24
Lee RosieShin So YoungKim Chun SooLee Hee JungByun Jun Chul - Soil heavy metal contamination has emerged as a critical global environmental issue due to industrialization, posing severe threats to human health. Notably, heavy metal pollution and herbicide application frequently coexist in agricultural systems. This study reveals enantiomer-specific effects of the widely used herbicide napropamide (NAP) on plant growth and cadmium (Cd) accumulation in Arabidopsis thaliana. Compared to the control, R-NAP enhanced plant growth while S-NAP exhibited inhibitory effects. Intriguingly, R-NAP treatment increased Cd accumulation by 14 % and 90 % relative to the control and S-NAP, respectively. Furthermore, R-NAP significantly elevated the contents of macronutrients (nitrogen (N), phosphorus (P), potassium (K), calcium (Ca), magnesium (Mg)) and micronutrients (iron (Fe), zinc (Zn)) by 1.05-1.3-fold and 1.25-1.82-fold compared to the control and S-NAP treatments. Mantel test and structural equation modeling (SEM) identified significant correlations between Cd and nutrients (N, P, Fe, Zn), with N and P directly/indirectly influencing Cd accumulation via Fe/Zn regulation. Transcriptomic analysis coupled with cross-domain network modeling uncovered core genes co-regulating nutrient uptake and Cd accumulation, including NRT1.2, NRT1.5, PHT3.2, ABCC9, and YSL6. Molecular docking confirmed strong binding affinities between NAP enantiomers and these transporter proteins. Our findings demonstrate that nutrient uptake dynamics mediate herbicide-induced Cd accumulation, providing novel insights for optimizing herbicide-nutrient management to mitigate crop metal uptake in contaminated farmlands. - Source: PubMed
Publication date: 2025/11/08
Zhu YaxinXie MinghuiCui HaoqiWu RanHuang LukuanWei QingLiu LijuanCai MiaozhenDu Shaoting