Table 1.

Summary of main effects of potassium channels in cancer cell chemoresistance.

K+ Channel	Cancer Models	Main Results	Relationship with Chemosensitivity	Ref.
Kv11.1 (hERG)	Various cancer cell lines (colorectal, breast, lung)	Positive correlation between level of expression and sensitivity to vincristine, camptothecin, or paclitaxel. Overexpression of Kv11.1 increased chemosensitivity.	More expression → more sensitivity	[25]
	gastric cancer (in vitro cell lines and in vivo mouse model)	Cisplatin increased Kv11.1 expression; Silencing Kv11.1 with siRNA decreased sensitivity to cisplatin by interfering with Bcl-2-dependent apoptosis.	Less expression/activity → less sensitivity	[26]
	Acute lymphoblastic leukemia (cell lines and primary cell culture, and in vivo mouse model)	Kv11.1 inhibition by blockers and siRNA reduced bone marrow mesenchymal cell-induced resistance of leukemic cells to doxorubicin, prednisone, or methotrexate.	Less expression/activity → more sensitivity	[27]
	colorectal cancer (in vitro cell lines and in vivo mouse model)	Increased expression/activity in cisplatin-resistant cell line; Inhibition of Kv11.1 increased cisplatin uptake and ciplastin-induced apoptosis in vitro, and overcome cisplatin resistance in vivo.	Less expression/activity → more sensitivity	[28]
Kv10.1 (hEag1)	Ovarian cancer (OC) (patient biopsies and cell lines)	Overall survival longer in cisplatin-treated OC patients with lower Kv10.1 expression; Silencing of Kv10.1 increased sensitivity to cisplatin by interfering with NFkB/Bcl-2 dependent apoptosis.	Less expression/activity → more sensitivity	[29]
	Hematological malignancies (patient biopsies, primary cells and cell lines)	Increased expression in acute myeloid leukemia patients predictive of a poor outcome; Kv10.1 inhibition by blockers or siRNA reduced cell proliferation and increased sensitivity to etoposide, cytarabine, or doxorubicin by promoting caspase activity.	Less expression/activity → more sensitivity	[30]
Kv1.5	Gastric cancer (cell lines)	Kv1.5 inhibition by K+ channel blocker or siRNA enhanced resistance to doxurubicin, 5-fluouracil, vincristine, or cisplatin, while Kv1.5 overexpression increased chemosensitivity.	Less expression/activity → less sensitivity More expression/activity → more sensitivity	[31]
Kv1.1, Kv1.3	Cancer cell line panel	Expression positively correlated with cisplatin-induced cell death.	More expression/activity → more sensitivity	[32]
KCa1.1 (BK)	Ovarian cancer (cell lines and primary cells)	KCa1.1 expression is inversely correlated with resistance to cisplatin; Channel knockdown by siRNA increased resistance to cisplatin.	Less expression/activity → less sensitivity	[33]
	Glioblastoma (cell line)	KCa1.1 promotes hypoxia-induced cell migration and resistance to cisplatin; KCa1.1 inhibition by paxilline increased sensitivity to cisplatin.	More expression/activity → less sensitivity Less expression/activity → more sensitivity	[34]
Kir2.1	Small cell lung cancer (patients, cell lines, and in vivo mouse model)	Increased Kir2.1 expression in patients’ cancer cells correlated with clinical stage progression and chemoresistance; Overexpression of Kir2.1 increased resistance to etoposide or cisplatin, whereas knockdown with siRNA increased chemosensitivity.	More expression/activity → less sensitivity Less expression/activity → more sensitivity	[35]