Reactive oxygen species and mitochondrial membrane potential are modulated during CDDP-induced apoptosis in EC-109 cellsThis paper is one of a selection of papers in this Special Issue, entitled International Symposium on Recent Advances in Molecular, Clinical, and Social Medicine, and has undergone the Journal's usual peer-review process.

Abstract

cis-Diamminedichloroplatinum (CDDP), commonly know as cisplatin, is a well known DNA-damaging agent, which is highly active in suppressing the proliferation of tumor cells. However, it is not clear that CDDP can induce growth inhibition of esophagus cancer cells. Using the cell line EC-109 from the esophagus, we found that CDDP would induce apoptotic responses. The addition of CDDP to cells led to the inhibition of growth in a time- and dose-dependent manner. CDDP generated reactive oxygen species (ROSs) in cells, which brought about a reduction in the intracellular mitochondrial transmembrane potential (Deltapsim), leading to apoptosis. Our findings demonstrate that ROSs, and the resulting oxidative stress, play a pivotal role in apoptosis. Preincubation of EC-109 cells with the hydrogen-peroxide-scavenging enzyme catalase partially inhibited the following: (i) the production of ROS; (ii) the disruption of the Deltapsim; and (iii) apoptosis. These results indicate that the enhancement of the generation of ROS and the disruption of Deltapsim are events involved in the apoptotic pathway of EC-109 induced by CDDP.

TRIM32 overexpression improves chemoresistance through regulation of mitochondrial function in non-small-cell lung cancers

“…However, excessive ROS could trigger apoptosis by altering the MMP and damaging the respiratory chain. 20 , 21 Our data demonstrated that TRIM32 had a protective role in cisplatin-induced ROS formation. To our knowledge, this is the first study to show the protective roles of TRIM32 on MMP and ROS in cisplatin-treated NSCLC cells.…”

Chemosensitization by phenothiazines in human lung cancer cells: impaired resolution of γH2AX and increased oxidative stress elicit apoptosis associated with lysosomal expansion and intense vacuolation

“…Many classes of DNA-damaging agents are known to induce oxidative stress, 13, 21, 22 which is a major cause for dysfunction of cellular organelles and cell death. 14, 23 Exposure of U1810 cells to bleomycin, cisplatin or TFP alone resulted in moderate increases of intracellular ROS (Figures 7a and b).…”

Rab18 overexpression promotes proliferation and chemoresistance through regulation of mitochondrial function in human gastric cancer

“…However, excessive ROS triggers apoptosis pathway by altering the MMP and damaging the respiratory chain. 17 , 18 Our data demonstrated that Rab18 had a protective role during CDDP-induced ROS formation. Considering the connection between ROS and MMP, it is possible that Rab18 inhibits CDDP-induced ROS production, which maintains MMP and reduces cytochrome c release, thus inhibiting CDDP-induced apoptosis.…”