Influence of Cx26/Cx32 gap junction channel on antineoplastic effect of etoposide in Hela cells.
- Author:
Xu-Hui TONG
1
;
Shu-Ying DONG
;
Guo-Jun JIANG
;
Gao-Fu FAN
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents, Phytogenic; pharmacology; Connexin 26; Connexins; genetics; metabolism; physiology; Etoposide; pharmacology; Gap Junctions; physiology; HeLa Cells; Humans; Transfection
- From: Journal of Southern Medical University 2012;32(3):329-332
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the influence of Cx26/Cx32 gap junction channel on the antineoplastic effect of etoposide in Hela cervical cancer cells.
METHODSFluorescence trace was used to assay the gap junction intercellular communication mediated by Cx26/Cx32 in Hela cells and its functional modulation by the pharmacological agents (oleamide, retinoid acid). A standard colony-forming assay was applied to determine the cell growth-inhibiting effect of etoposide in Hela cells with functional modulation of the gap junction. Hoechst 33258 staining was used to assess the changes in etoposide-induced apoptosis of Hela cells with altered gap junction functions.
RESULTSOleamide markedly decreased while retinoid acid obviously increased the gap junction function in Hela cells. Standard colony-forming assay showed that etoposide produced a lowered antiproliferative effect in Hela cells with reduced gap junction and an increased antiproliferative effect in cells with enhanced gap junction function. In cells with a reduced gap junction function, etoposide induced a lowered apoptosis rate, which increased obviously in cells with an enhanced gap junction function.
CONCLUSIONThe antineoplastic effect of etoposide is reduced in Hela cells with a decreased gap junction intercellular communication mediated by Cx26/Cx32 and is enhanced in cells with an increased gap junction intercellular communication.