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Biochemical Inhibition of DOG1/TMEM16A Achieves Antitumoral Effects in Human Gastrointestinal Stromal Tumor Cells In Vitro
Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.ORCID iD: 0000-0002-9742-244X
Karolinska Inst, Rolf Luft Ctr Diabet Res, Dept Mol Med & Surg, Stockholm, Sweden.
Karolinska Inst, Rolf Luft Ctr Diabet Res, Dept Mol Med & Surg, Stockholm, Sweden.
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2019 (English)In: Anticancer Research, ISSN 0250-7005, E-ISSN 1791-7530, Vol. 39, no 7, p. 3433-3442Article in journal (Refereed) Published
Abstract [en]

Background/Aim: DOG1 is a calcium-activated chloride channel that has gained attention as a promising drug target due to its involvement in several processes essential for tumor development and progression. DOG1 is overexpressed in >95% of gastrointestinal stromal tumors (GIST). The aim was to determine DOG1 inhibition antitumoral effects on GIST. Materials and Methods: Human GIST (GIST-T1 and GIST882) cell lines were used to study the effect of DOG1 inhibitors on chloride currents, viability, colony formation, and cell cycle. Results: CaCCinh-A01 decreased chloride currents. CaCCinh-A01 and T16(inh)-A01 reduced GIST cell viability and CaCCinh-A01 affected cell cycle distribution leading to G(1) cell-cycle arrest. CaCCinh-A01 also increased the sub-G(1) phase population, indicative of apoptosis, in GIST882. CaCCinh-A01 strongly reduced the colony forming ability of the cells, whereas T16(inh)-A01 did not. Conclusion: DOG1 inhibition has antitumoral effects in GIST cells in vitro, and could potentially serve as a target for GIST therapy.

Place, publisher, year, edition, pages
INT INST ANTICANCER RESEARCH , 2019. Vol. 39, no 7, p. 3433-3442
Keywords [en]
Gastrointestinal stromal tumors, GIST, DOG1, TMEM16A, ion channel, cancer
National Category
Cancer and Oncology
Identifiers
URN: urn:nbn:se:uu:diva-393835DOI: 10.21873/anticanres.13489ISI: 000482700300019PubMedID: 31262867OAI: oai:DiVA.org:uu-393835DiVA, id: diva2:1355354
Funder
Swedish Research CouncilAvailable from: 2019-09-27 Created: 2019-09-27 Last updated: 2019-09-27Bibliographically approved

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