Subunits of BK channels promote breast cancer development and modulate responses to endocrine treatment in preclinical models.

Background And Purpose: Pore-forming α subunits of the voltage- and Ca -activated K channel with large conductance (BKα) promote malignant phenotypes of breast tumour cells. Auxiliary subunits such as the leucine-rich repeat containing 26 (LRRC26) protein, also termed BKγ1, may be required to permit activation of BK currents at a depolarized resting membrane potential that frequently occur in non-excitable tumour cells.

Experimental Approach: Anti-tumour effects of BKα loss were investigated in breast tumour-bearing MMTV-PyMT transgenic BKα knockout (KO) mice, primary MMTV-PyMT cell cultures, and in a syngeneic transplantation model of breast cancer derived from these cells.

K3.1 Channels Confer Radioresistance to Breast Cancer Cells.

K3.1 K channels reportedly contribute to the proliferation of breast tumor cells and may serve pro-tumor functions in the microenvironment. The putative interaction of K3.

From in vitro to ex vivo: subcellular localization and uptake of graphene quantum dots into solid tumors.

Among various nanoparticles tested for pharmacological applications over the recent years, graphene quantum dots (GQDs) seem to be promising candidates for the construction of drug delivery systems due to their superior biophysical and biochemical properties. The subcellular fate of incorporated nanomaterial is decisive for transporting pharmaceuticals into target cells. Therefore a detailed characterization of the uptake of GQDs into different breast cancer models was performed.

Cancer-Associated Intermediate Conductance Ca-Activated K⁺ Channel K3.1.

Several tumor entities have been reported to overexpress K3.1 potassium channels due to epigenetic, transcriptional, or post-translational modifications. By modulating membrane potential, cell volume, or Ca signaling, K3.

SK4 channels modulate Ca signalling and cell cycle progression in murine breast cancer.

Oncogenic signalling via Ca -activated K channels of intermediate conductance (SK4, also known as K 3.1 or IK) has been implicated in different cancer entities including breast cancer. Yet, the role of endogenous SK4 channels for tumorigenesis is unclear.