Published online Apr 28, 2021. doi: 10.3748/wjg.v27.i16.1805
Peer-review started: January 8, 2021
First decision: February 11, 2021
Revised: February 14, 2021
Accepted: March 24, 2021
Article in press: March 24, 2021
Published online: April 28, 2021
Esophageal cancer is a malignant tumor of the digestive tract that is difficult to diagnose early. Although CPI-455 is reported to inhibit various cancers, the role of CPI-455 in esophageal squamous cell carcinoma (ESCC) is unknown.
KDM5C, a lysine-specific demethylase 5C, inhibited ESCC proliferation and invasion, which may be partly associated with the expression of p53, Bax, Caspase-9, and Caspase-3. Mitochondria-mediated intrinsic apoptotic signaling plays an important role in the process of Eca-109 cell apoptosis induced by CPI-455.
The study objective was to investigate the effect and mechanism of the KDM5C inhibitor, CPI-455, on ESCC cells.
The changes in proliferation, apoptosis, ROS content, and mitochondrial membrane potential of Eca-109 cells induced by CPI-455 were observed. The expression of P53, Bax, Caspase-9, Caspase-3, and KDM5C in Eca-109 cells was assayed.
CPI-455 inhibited Eca-109 cell proliferation. P53, Bax, Caspase-9, and Caspase-3 were upregulated in Eca-109 cells, and KDM5C was significantly downregulated, by CPI-455. CPI-455 increased the level of intracellular ROS in Eca-109 cells, and decreased the mitochondrial membrane potential compared with the control group.
CPI-455 inhibited Eca-109 cell proliferation via the mitochondrial apoptosis pathway by regulating the expression of related genes.
CPI-455 might be a potential candidate for the development of novel chemothera