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Pharmacologic inducers of the uric acid exporter ABCG2 as potential drugs for treatment of gouty arthritis

Asian Journal of Pharmaceutical Sciences 2020年第2期15卷 173-180页

作者： Bojana Ristic Mohd Omar Faruk Sikder Yangzom D.Bhutia vadivel ganapathy Department of Cell Biology and Biochemistry Texas Tech University Health Sciences CenterLubbockTX 79430United States

Uric acid is the end product of purine catabolism and its plasma levels are maintained below its maximum solubility in water(6–7 mg/dl).The plasma levels are tightly regulated as the balance between the rate of production and the rate of excretion,the latter occurring in urine(kidney),bile(liver)and feces(intestinal tract).Reabsorption in kidney is also an important component of this *** excretion and reabsorption are mediated by specific *** of the balance between production and excretion leads to hyperuricemia,which increases the risk of uric acid crystallization as monosodium urate with subsequent deposition of the crystals in joints causing gouty ***-of-function mutations in the transporters that mediate uric acid excretion are associated with *** ATP-Binding Cassette exporter ABCG2 is important in uric acid excretion at all three sites:kidney(urine),liver(bile),and intestine(feces).Mutations in this transporter cause gout and these mutations occur at significant prevalence in general ***,mutations that are most prevalent result only in partial loss of transport ***,if the expression of these partially defective transporters could be induced,the increased number of the transporter molecules would compensate for the mutation-associated decrease in transport function and hence increase uric acid *** such,pharmacologic agents with ability to induce the expression of ABCG2 represent potentially a novel class of drugs for treatment of gouty arthritis.

关键词： Uric acid excretion Intestine ABCG2 Loss-of-function mutations Gouty arthritis Pharmacologic inducers

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The amino acid transporter SLC6A14 in cancer and its potential use in chemotherapy

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Asian Journal of Pharmaceutical Sciences 2014年第6期9卷 293-303页

作者： Yangzom D.Bhutia Ellappan Babu Puttur D.Prasad vadivel ganapathy Department of Biochemistry and Molecular Biology Medical College of GeorgiaGeorgia Regents UniversityAugustaGA 30912USA

Tumor cells have an increased demand for glucose and amino acids to support their rapid growth,and also exhibit alterations in biochemical pathways that metabolize these *** across the plasma membrane is essential to feed glucose and amino acids into these tumor cell-selective metabolic *** of amino acids across biological membranes occurs via a multitude of transporters;tumor cells must upregulate one or more of these transporters to satisfy their increased demand for amino *** the amino acid transporters,SLC6A14 stands out with specific functional features uniquely suited for the biological needs of the tumor *** transporter is indeed upregulated in tumors of epithelial origin,including colon cancer,cervical cancer,breast cancer,and pancreatic *** normal cells express this transporter only at low levels,blockade of this transporter should lead to amino acid starvation selectively in tumor cells,thus having little effect on normal *** offers a novel,yet logical,strategy for the treatment of cancers that are associated with upregulation of *** addition,a variety of amino acid-based prodrugs are recognized as substrates by SLC6A14,thus raising the possibility that anticancer drugs can be delivered into tumor cells selectively via this transporter in the form of amino acid *** strategy allows exposure of SLC6A14-positive tumor cells to chemotherapy with minimal off-target *** conclusion,the amino acid transporter SLC6A14 holds great potential not only as a direct drug target for cancer therapy but also for tumor cell-selective delivery of anticancer drugs.

关键词： Essential amino acids Glutamine addiction Amino acid transporters SLC6A14 Prodrugs Cancer therapy

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Resetting amino acid metabolism of cancer cells by ATB^(0,+)-targeted nanoparticles for enhanced anticancer therapy

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Bioactive Materials 2022年第3期7卷 15-28页

作者： Longfa Kou Xinyu Jiang Yingying Tang Xing Xia Yingtao Li Aimin Cai Hailun Zheng Hailin Zhang vadivel ganapathy Qing Yao Ruijie Chen Department of Pharmacy The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhou325027China School of Pharmaceutical Sciences Wenzhou Medical UniversityWenzhou325035China Department of Children’s Respiration Disease The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhou325027China Department of Cell Biology and Biochemistry Texas Tech University Health Sciences CenterLubbockTX79430USA

Reprogramed cellular metabolism is one of the most significant hallmarks of *** cancer cells exhibit increased demand for specific amino acids,and become dependent on either an exogenous supply or upregulated de novo *** resultant enhanced availability of amino acids supports the reprogramed metabolic pathways and fuels the malignant growth and metastasis of cancers by providing energy and critical metabolic intermediates,facilitating anabolism,and activating signaling networks related to cell proliferation and ***,pharmacologic blockade of amino acid entry into cancer cells is likely to have a detrimental effect on cancer cell *** we developed a nanoplatform(LJ@Trp-NPs)to therapeutically target two transporters,SLC6A14(ATB^(0,+))and SLC7A5(LAT1),that are known to be essential for the sustenance of amino acid metabolism in most *** LJ@Trp-NPs uses tryptophan to guide SLC6A14-targeted delivery of JPH203,a high-affinity inhibitor of *** the process,SLC6A14 is also *** tested the ability of this strategy to synergize with the anticancer efficacy of lapatinib,an inhibitor of EGFR/HER1/HER2-assocated *** studies show that blockade of amino acid entry amplifies the anticancer effect of lapatinib via interference with mTOR signaling,promotion of apoptosis,and suppression of cell proliferation and *** represents the first study to evaluate the impact of amino acid starvation on the anticancer efficacy of widely used kinase inhibitor.

关键词： Amino acid delivery ATB^(0,+)targeting Nanoparticles Cancer therapy mTOR

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Chronic exposure to excess iron promotes EMT and cancer via p53 loss in pancreatic cancer

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Asian Journal of Pharmaceutical Sciences 2020年第2期15卷 237-251页

作者： Yangzom D.Bhutia Jiro Ogura Paul J.Grippo Carolina Torres Toshihiro Sato Mitchell Wachtel Sabarish Ramachandran Ellappan Babu Sathish Sivaprakasam Devaraja Rajasekaran Bradley Schniers Nhu On Logan Smoot Muthusamy Thangaraju Jaya P.Gnana-Prakasam vadivel ganapathy Department of Cell Biology and Biochemistry Texas Tech University Health Sciences CenterLubbockTX 79430USA Department of Pharmaceutical Sciences Tohoku University Hospital1-1 Seiryo-machiAoba-kuSendaiMiyagi 980-8574Japan Department of Medicine University of Illinois at ChicagoChicagoIL 60607USA Department of Surgical Pathology Texas Tech University Health Sciences CenterLubbockTX 79430USA Department of Biological Sciences Texas Tech UniversityLubbockTX 79410USA Department of Chemistry and Biochemistry Texas Tech UniversityLubbockTX 79410USA Department of Biochemistry and Molecular Biology Augusta UniversityAugustaGA 30912USA Department of Ophthalmology St.Louis UniversitySt.LouisMO 63104USA

Based on the evidence that hemochromatosis, an iron-overload disease, drives hepatocellular carcinoma, we hypothesized that chronic exposure to excess iron, either due to genetic or environmental causes, predisposes an individual to cancer. Using pancreatic cancer as our primary focus, we employed cell culture studies to interrogate the connection between excess iron and cancer, and combined in vitro and in vivo studies to explore the connection further. Ferric ammonium citrate was used as an exogenous iron source. Chronic exposure to excess iron induced epithelial-mesenchymal transition(EMT) in normal and cancer cell lines, loss of p53, and suppression of p53 transcriptional activity evidenced from decreased expression of p53 target genes(p21, cyclin D1, Bax, SLC7A11). To further extrapolate our cell culture data, we generated EL-KrasG12D( EL-Kras) mouse(pancreatic neoplastic mouse model) expressing Hfe+/+ and Hfe-/- genetic background. p53 target gene expression decreased in EL-Kras/Hfe-/- mouse pancreas compared to EL-Kras/Hfe+/+ mouse pancreas. Interestingly, the incidence of acinar-to-ductal metaplasia and cystic pancreatic neoplasms(CPN) decreased in EL-Kras/Hfe-/- mice, but the CPNs that did develop were larger in these mice than in EL-Kras/Hfe+/+ mice. In conclusion, these in vitro and in vivo studies support a potential role for chronic exposure to excess iron as a promoter of more aggressive disease via p53 loss and SLC7A11 upregulation within pancreatic epithelial cells.

关键词： SLC7A11 p53 Iron Heme Epithelial-mesenchymal transition

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