title: Stimulation of beta-adrenoceptor enhances sensitivity to cisplatin in non-small cell lung cancer cell lines.
abstract: Cisplatin is a key drug in chemotherapy for lung cancer. It has been reported that intracellular accumulation of cisplatin is an important step as a determinant for resistance to cisplatin, which may be modulated by Na+, K+-ATPase activity. And it has been reported that beta-adrenoceptor agonists modulate the Na+, K+-ATPase in some organs. In this study, the effects of a beta-adrenoceptor agonist and an antagonist on membrane Na+, K+-ATPase activity were evaluated using human non-small cell (NSCLC) lung cancer cell lines. In the NSCLC cell lines, sensitivity to cisplatin was improved by treatment with isoproterenol. Na+, K+-ATPase was activated and intracellular accumulation of cisplatin increased with the treatment. But the antagonist, propranolol, did not modulate sensitivity to cisplatin or Na+, K+-ATPase activity. These results suggest that beta-adrenoceptors may be one of the determinant for sensitivity to cisplatin in NSCLC, but endogenous catecholamine dose not play a role in the intracellular accumulation of cisplatin in these cell lines. Exogenous beta-adrenoceptor agonists may improve the antitumor effect of chemotherapy involving cisplatin.
authors.forename: T
authors.initials: T
authors.lastname: Bando
authors.forename: M
authors.initials: M
authors.lastname: Fujimura
authors.forename: K
authors.initials: K
authors.lastname: Kasahara
authors.forename: K
authors.initials: K
authors.lastname: Shibata
authors.forename: H
authors.initials: H
authors.lastname: Shirasaki
authors.forename: U
authors.initials: U
authors.lastname: Heki
authors.forename: K
authors.initials: K
authors.lastname: Iwasa
authors.forename: A
authors.initials: A
authors.lastname: Ueda
authors.forename: S
authors.initials: S
authors.lastname: Tomikawa
authors.forename: T
authors.initials: T
authors.lastname: Matsuda