The combined activation of K_Ca3.1 and inhibition of K_v11.1/hERG1 currents contribute to overcome Cisplatin resistance in colorectal cancer cells.

ABSTRACT:

Background

Platinum-based drugs such as Cisplatin are commonly employed for cancer treatment. Despite an initial therapeutic response, Cisplatin treatment often results in the development of chemoresistance. To identify novel approaches to overcome Cisplatin resistance, we tested Cisplatin in combination with K⁺ channel modulators on colorectal cancer (CRC) cells.

Methods

The functional expression of Ca²⁺-activated (K_Ca3.1, also known as KCNN4) and voltage-dependent (K_v11.1, also known as KCNH2 or hERG1) K⁺ channels was determined in two CRC cell lines (HCT-116 and HCT-8) by molecular and electrophysiological techniques. Cisplatin and several K⁺ channel modulators were tested in vitro for their action on K

SUBMITTER: Pillozzi S 

PROVIDER: S-EPMC5785745 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature