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World J Gastroenterol. Aug 28, 2026; 32(32): 118600
Published online Aug 28, 2026. doi: 10.3748/wjg.118600
Published online Aug 28, 2026. doi: 10.3748/wjg.118600
Pristimerin attenuates spasmolytic polypeptide-expressing metaplasia via p57 (Cdkn1c)-mediated glycolytic reprogramming: A metabolic avenue for gastric cancer prevention
Jun-Hao Han, Kong-Rui Lu, Min Zhang, Guo-Hua Gong, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China
Author contributions: Han JH wrote the manuscript; Zhang M and Lu KR designed the figure; Gong GH conceived the idea and revised the manuscript.
AI contribution statement: For the manuscript text, the author used DeepSeek to assist with language polishing and to screen for typos. The logical structure, main arguments, literature search, citation and figures, as well as the final version of the manuscript, were all completed independently by the author, who takes full responsibility for the content of this paper.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Corresponding author: Guo-Hua Gong, PhD, Professor, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, No. 82 West College Road, Wenzhou 325035, Zhejiang Province, China. guohgong@wmu.edu.cn
Received: January 7, 2026
Revised: March 9, 2026
Accepted: May 28, 2026
Published online: August 28, 2026
Processing time: 207 Days and 5.5 Hours
Revised: March 9, 2026
Accepted: May 28, 2026
Published online: August 28, 2026
Processing time: 207 Days and 5.5 Hours
Core Tip
Core Tip: This opinion review discusses evidence that the natural compound pristimerin reverses spasmolytic polypeptide-expressing metaplasia (SPEM) not only by alleviating high-dose tamoxifen-induced gastric mucosal injury and oxyntic atrophy, but also by restoring parietal and chief cell lineages and suppressing aberrant proliferation. The study further identifies Cdkn1c (p57) as a key metabolic checkpoint: p57 is downregulated during SPEM, upregulated following pristimerin treatment, and required for the compound’s antiglycolytic and anti-SPEM effects in gastric organoids.