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Cl− and K+ channels in human pancreatic ductal adenocarcinoma (PDAC) cells
Author(s) -
Sauter Daniel Rafael Peter,
Pedersen Stine Falsig,
Novak Ivana,
Larsen Erik Hviid,
Hoffmann Else Kay
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.913.17
Subject(s) - pancreatic cancer , cancer research , metastasis , cell growth , cell culture , skbr3 , medicine , cancer , cancer cell , endocrinology , chemistry , biology , biochemistry , human breast , genetics
The Cl‐ channel anoctamin‐1 (ANO1 or TMEM16A) is overexpressed in oral, head, prostate and colon cancer and predicted as a pharmaceutical target or biomarker for distant metastasis. The K2p K+ channel family (e.g. TREKs, TWIKs, and TASKs) is also associated with the pathogenesis of cancer. ANO1 and the K2p channels are involved in regulation of cell migration, cell volume, and apoptosis and might contribute to cancer development through modulating these processes. Here, we aim at determining the roles of ANO1 and K2p channels in pancreatic ductal adenocarcinoma (PDAC). Channel expression levels in 4 human PDAC lines (AsPC‐1, BxPC‐3, PANC‐1, MIAPaCa‐2) were compared to the normal pancreatic ductal epithelial cell line (HPDE*) by qPCR analysis. We found ANO1, TWIK‐1, TREK‐1 and TASK‐3 to be over‐expressed in PDAC cells. Whole‐cell patch‐clamp measurements of ANO1 in AsPC‐1 cells revealed a time‐, voltage‐and temperature dependent Cl‐ current with the instantaneous ICl/V relationship exhibiting GHK‐rectification. ANO1‐like currents were in our experiments not recorded in HPDE cells. We conclude that ANO1 upregulation may be a marker in pancreatic cancer cell lines, however, its function is yet unknown and ongoing studies evaluate the potential roles of ANO1 in PDAC growth and chemotherapy resistance. Financed by FP7 Marie Curie Initial Training Network “IonTraC”.