PT - JOURNAL ARTICLE AU - ROBIN FRÖBOM AU - FELIX SELLBERG AU - CHENG XU AU - ALLAN ZHAO AU - CATHARINA LARSSON AU - WENN-ONN LUI AU - INGA-LENA NILSSON AU - ERIK BERGLUND AU - ROBERT BRÄNSTRÖM TI - Biochemical Inhibition of DOG1/TMEM16A Achieves Antitumoral Effects in Human Gastrointestinal Stromal Tumor Cells <em>In Vitro</em> AID - 10.21873/anticanres.13489 DP - 2019 Jul 01 TA - Anticancer Research PG - 3433--3442 VI - 39 IP - 7 4099 - http://ar.iiarjournals.org/content/39/7/3433.short 4100 - http://ar.iiarjournals.org/content/39/7/3433.full SO - Anticancer Res2019 Jul 01; 39 AB - 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 &gt;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 T16inh-A01 reduced GIST cell viability and CaCCinh-A01 affected cell cycle distribution leading to G1 cell-cycle arrest. CaCCinh-A01 also increased the sub-G1 phase population, indicative of apoptosis, in GIST882. CaCCinh-A01 strongly reduced the colony forming ability of the cells, whereas T16inh-A01 did not. Conclusion: DOG1 inhibition has antitumoral effects in GIST cells in vitro, and could potentially serve as a target for GIST therapy.