Clin Oncol | Volume 8, Issue 1 | Research Article | Open Access
Zhaozu F1, Ke W2, Yunfengc M3 and Wenjuan L2*
1Department of Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, China 2Medicine School of Xi'an Jiaotong University, China 3Department of Pathogenic Biology and Immunology, Medicine School of Xi'an Jiaotong University, China
*Correspondance to: Luo WenjuanFulltext PDF
Objective: Carfilzomib induces endometrial carcinoma cell apoptosis by activating the endoplasmic reticulum stress signaling pathway. Methods: Two endometrial cancer cell lines, HEC-1-A and Ishikawa, were treated with Carfilzomib. Flow cytometry was used to detect cancer cell apoptosis at different concentrations and times. The expression of GRP78 and CHOP genes in endoplasmic reticulum stress was detected by qRT-PCR. Western Blot method was used to examine the effect of Carfilzomib on the expression of apoptosispromoting factors (Bim, Puma, Noxa, and Bax) and endoplasmic reticulum stress-related factors (GRP78 and CHOP) in endometrial cancer cells. Results: Flow cytometry showed that Carfilzomib time- and dose-dependently induced the apoptosis of two endometrial cancer cell lines. qRT-PCR showed that Carfilzomib significantly upregulated GRP78 and CHOP expression. Western blot showed that the apoptosis-promoting factors Bim, Puma and Noxa were upregulated at the protein level, while changes in GRP78 and CHOP were dose-dependent. Conclusion: The effect of Carfilzomib on endometrial cancer cells shows that the drug causes tumor cell apoptosis through the activation of the endoplasmic reticulum stress signal pathway in cancer cells.
Zhaozu F, Ke W, Yunfengc M, Wenjuan L. Carfilzomib Induces Apoptosis of Endometrial Carcinoma Cells by Activating Endoplasmic Reticulum Stress. Clin Oncol. 2023;8:1982.