Chen JY, Li JD, He RQ, Huang ZG, Chen G, Zou W. Bibliometric analysis of phosphoglycerate kinase 1 expression in breast cancer and its distinct upregulation in triple-negative breast cancer. World J Clin Oncol 2024; 15(7): 867-894 [DOI: 10.5306/wjco.v15.i7.867]
Corresponding Author of This Article
Wen Zou, MM, Doctor, Department of Pathology, First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning 530021, Guangxi Zhuang Autonomous Region, China. pathologyzw@sr.gxmu.edu.cn
Research Domain of This Article
Oncology
Article-Type of This Article
Clinical and Translational Research
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Oncol. Jul 24, 2024; 15(7): 867-894 Published online Jul 24, 2024. doi: 10.5306/wjco.v15.i7.867
Bibliometric analysis of phosphoglycerate kinase 1 expression in breast cancer and its distinct upregulation in triple-negative breast cancer
Jing-Yu Chen, Jian-Di Li, Rong-Quan He, Zhi-Guang Huang, Gang Chen, Wen Zou
Jing-Yu Chen, Jian-Di Li, Zhi-Guang Huang, Gang Chen, Wen Zou, Department of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Rong-Quan He, Department of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Author contributions: He RQ, Huang ZG, Chen G, and Zou W designed the paper; Chen JY and Li JD performed literature and dataset screening, conducted bibliometric statistics, and carried out all computational analyses, including mRNA and protein expression, prognosis and signaling pathways; Chen JY, Li JD, Huang ZG, and Zou W constructed the figures and tables; Chen JY and Li JD wrote the draft; He RQ, Huang ZG, Chen G, and Zou W corrected the draft; and all authors have read and approved the final manuscript.
Supported bythe Guangxi Zhuang Autonomous Region Health Commission Scientific Research Project, No. Z-A20220530.
Conflict-of-interest statement: All the authors declare no competing financial interests.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Wen Zou, MM, Doctor, Department of Pathology, First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning 530021, Guangxi Zhuang Autonomous Region, China. pathologyzw@sr.gxmu.edu.cn
Received: February 8, 2024 Revised: May 27, 2024 Accepted: June 24, 2024 Published online: July 24, 2024 Processing time: 159 Days and 0.2 Hours
Abstract
BACKGROUND
Phosphoglycerate kinase 1 (PGK1) has been identified as a possible biomarker for breast cancer (BC) and may play a role in the development and advancement of triple-negative BC (TNBC).
AIM
To explore the PGK1 and BC research status and PGK1 expression and mechanism differences among TNBC, non-TNBC, and normal breast tissue.
METHODS
PGK1 and BC related literature was downloaded from Web of Science Core Collection Core Collection. Publication counts, key-word frequency, cooperation networks, and theme trends were analyzed. Normal breast, TNBC, and non-TNBC mRNA data were gathered, and differentially expressed genes obtained. Area under the summary receiver operating characteristic curves, sensitivity and specificity of PGK1 expression were determined. Kaplan Meier revealed PGK1’s prognostic implication. PGK1 co-expressed genes were explored, and Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Disease Ontology applied. Protein-protein interaction networks were constructed. Hub genes identified.
RESULTS
PGK1 and BC related publications have surged since 2020, with China leading the way. The most frequent keyword was “Expression”. Collaborative networks were found among co-citations, countries, institutions, and authors. PGK1 expression and BC progression were research hotspots, and PGK1 expression and BC survival were research frontiers. In 16 TNBC vs non-cancerous breast and 15 TNBC vs non-TNBC datasets, PGK1 mRNA levels were higher in 1159 TNBC than 1205 non-cancerous breast cases [standardized mean differences (SMD): 0.85, 95% confidence interval (95%CI): 0.54-1.16, I² = 86%, P < 0.001]. PGK1 expression was higher in 1520 TNBC than 7072 non-TNBC cases (SMD: 0.25, 95%CI: 0.03-0.47, I² = 91%, P = 0.02). Recurrence free survival was lower in PGK1-high-expression than PGK1-low-expression group (hazard ratio: 1.282, P = 0.023). PGK1 co-expressed genes were concentrated in ATP metabolic process, HIF-1 signaling, and glycolysis/gluconeogenesis pathways.
CONCLUSION
PGK1 expression is a research hotspot and frontier direction in the BC field. PGK1 may play a strong role in promoting cancer in TNBC by mediating metabolism and HIF-1 signaling pathways.
Core Tip: The expression of phosphoglycerate kinase 1 (PGK1) in breast cancer (BC) was shown to be both a research hotspot and frontier of BC research. PGK1 mRNA levels were significantly higher in triple-negative BC (TNBC) than in non-cancerous breast tissue. Within the population with BC, PGK1 mRNA expression levels were distinctly upregulated in TNBC compared with non-TNBC. Recurrence-free survival was markedly lower in the PGK1-high-expression than the PGK1-low-expression group. PGK1 has a significant role in promoting TNBC through metabolism and HIF-1 signaling pathways.
