Role of Ca2+-activated K+ Channels in Breast Cancer Proliferation and Resistance to Cytotoxic Drugs and Radiation

• Applicant: Professor Dr. Peter Ruth
• Subject Area: Pharmacology
• Term: from 2014 to 2019
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 248631763

• Final Report Year: 2020

Final Report Abstract

Our findings provide important new knowledge with regards to the in vivo biological role of BKα and BKγ1 in breast cancer onset and progression supporting the notion that both BK and BKα/γ1 may be suitable pharmacological targets for breast cancer. To this end, we suggest, that given BKα’s pleiotropic functions and expected multiple adverse effects upon global channel inhibition, a targeting of epithelial and cancer-associated BKα/γ1 complexes may offer a suitable opportunity to develop tolerable treatments that may be useful in combination with antihormonal treatment.

Publications

• (2017) SK4 channels modulate Ca2+ signalling and cell cycle progression in murine breast cancer. Mol Oncol. 11, 1172-1188
  Steudel FA, Mohr CJ, Stegen B, Nguyen HY, Barnert A, Steinle M, Beer-Hammer S, Koch P, Lo WY, Schroth W, Hoppe R, Brauch H, Ruth P, Huber SM, Lukowski R
  
• (2019) Cancer-Associated Intermediate Conductance Ca2+-Activated K⁺ Channel KCa3.1. Cancers 11, E109
  Mohr CJ, Steudel FA, Gross D, Ruth P, Lo WY, Hoppe R, Schroth W, Brauch H, Huber SM, Lukowski R
  
• (2019) KCa3.1 Channels Confer Radioresistance to Breast Cancer Cells. Cancers 11, E1285
  Mohr CJ, Gross D, Sezgin EC, Steudel FA, Ruth P, Huber SM, Lukowski R