Preliminary Evaluation of the Anticancer Activity of a PGK1 Small Molecule Inhibitor in Ishikawa Endometrial Cancer
- 1NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China
- 2School of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing 210023, China
- 3State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China
Abstract
To investigate the roles of a phosphoglycerate kinase 1 (PGK1) small-molecule inhibitor in Ishikawa endometrial cancer. The role of a PGK1 small molecule inhibitor in endometrial cancer was identified by cell viability, transwell, cell cycle, and apoptosis analyses. The expression levels of PGK1 in cancer cells treated with various concentrations of the PGK1 small molecule inhibitor at 48 h and 72 h were determined via Western blotting. Xenograft mouse models were established through subcutaneous tumor transplantation, and immunofluorescence analysis of PGK1 and apoptosis in tumor tissue was performed. The results of the cell counting kit-8 (CCK-8) assay revealed that NG52 inhibited the activity of human endometrial carcinoma Ishikawa, HEC-1-A, and HEC-1-B cells in a concentration-dependent manner. Moreover, NG52 significantly reduced the migration ability of the Ishikawa cell line in a dose-dependent manner. Flow cytometry (FCM) demonstrated that NG52 affected the survival of endometrial carcinoma cells by arresting the cell cycle at the G1 phase and inducing apoptosis in a dose-dependent manner. Western blot analysis also revealed that the apoptosis-inducing effects of NG52 were accompanied by a reduction in PGK1 expression after 48 h and 72 h of NG52 treatment. Moreover, NG52 partially suppressed tumor growth in a human Ishikawa xenograft model, and transferase dUTP nick end labeling (TUNEL) showed an increasing trend of NG52-treated tumor tissue apoptosis, with a decreasing trend in PGK1 expression in the treatment group. NG52, a PGK1 small molecule inhibitor, can serve as a structural basis for developing potential anti-endometrial carcinoma agents. The findings are limited to the preliminary preclinical activity of NG52, and further mechanistic, pharmacologic, efficacy, and safety studies are warranted before improved PGK1 inhibitors can proceed to clinical translation.
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BibTeX
@article{cao2026preliminary,
title = {{Preliminary Evaluation of the Anticancer Activity of a PGK1 Small Molecule Inhibitor in Ishikawa Endometrial Cancer}},
author = {Haijing Cao and Shengyu Xue and Man Xue and Fang Li and Linglin Feng and Wei Zheng and Hong Ding and Ting Zhang},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219641},
url = {https://www.mdpi.com/1422-0067/27/21/9641},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Preliminary Evaluation of the Anticancer Activity of a PGK1 Small Molecule Inhibitor in Ishikawa Endometrial Cancer
AU - Haijing Cao
AU - Shengyu Xue
AU - Man Xue
AU - Fang Li
AU - Linglin Feng
AU - Wei Zheng
AU - Hong Ding
AU - Ting Zhang
PY - 2026
DA - 2026/10/28
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219641
UR - https://www.mdpi.com/1422-0067/27/21/9641
AB - To investigate the roles of a phosphoglycerate kinase 1 (PGK1) small-molecule inhibitor in Ishikawa endometrial cancer. The role of a PGK1 small molecule inhibitor in endometrial cancer was identified by cell viability, transwell, cell cycle, and apoptosis analyses. The expression levels of PGK1 in cancer cells treated with various concentrations of the PGK1 small molecule inhibitor at 48 h and 72 h were determined via Western blotting. Xenograft mouse models were established through subcutaneous tumor transplantation, and immunofluorescence analysis of PGK1 and apoptosis in tumor tissue was performed. The results of the cell counting kit-8 (CCK-8) assay revealed that NG52 inhibited the activity of human endometrial carcinoma Ishikawa, HEC-1-A, and HEC-1-B cells in a concentration-dependent manner. Moreover, NG52 significantly reduced the migration ability of the Ishikawa cell line in a dose-dependent manner. Flow cytometry (FCM) demonstrated that NG52 affected the survival of endometrial carcinoma cells by arresting the cell cycle at the G1 phase and inducing apoptosis in a dose-dependent manner. Western blot analysis also revealed that the apoptosis-inducing effects of NG52 were accompanied by a reduction in PGK1 expression after 48 h and 72 h of NG52 treatment. Moreover, NG52 partially suppressed tumor growth in a human Ishikawa xenograft model, and transferase dUTP nick end labeling (TUNEL) showed an increasing trend of NG52-treated tumor tissue apoptosis, with a decreasing trend in PGK1 expression in the treatment group. NG52, a PGK1 small molecule inhibitor, can serve as a structural basis for developing potential anti-endometrial carcinoma agents. The findings are limited to the preliminary preclinical activity of NG52, and further mechanistic, pharmacologic, efficacy, and safety studies are warranted before improved PGK1 inhibitors can proceed to clinical translation.
SN - 1422-0067
ER -