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Updated: Oct 16, 2026

Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker
Published on: September 15, 2023
PTTG1 drives intestinal-type gastric cancer progression via G2/M checkpoint-mediated cell-cycle reprogramming
Caihong Hu1,2, Lijun Bian2,3, Lin Luo2
1Department of Epidemiology, School of Public Health, Southeast University, Nanjing, China.
Abstract:
Intestinal-type gastric cancer (IGC) progresses through the Correa cascade, yet the molecular determinants of this transition remain insufficiently defined. Using single-cell RNA sequencing (scRNA-seq) on matched normal, intestinal metaplasia, and tumor tissues from five patients, we identified eight epithelial subtypes, including a transitional enterocyte population that expanded along the disease trajectory. Pseudotime and network analyses revealed a progressive upregulation of PTTG1, which was further supported by public cohorts, bulk transcriptomics, and tissue microarrays. Functional assays demonstrated that PTTG1 knockdown impaired G2/M checkpoint regulation and reduced gastric cancer cell proliferation, migration, and invasion, whereas its overexpression enhanced organoid growth and altered mucin-related features. In xenograft models, PTTG1 depletion suppressed tumor growth and was accompanied by secretory differentiation-associated histological changes. Collectively, these findings suggest that PTTG1 contributes to intestinal-type gastric cancer progression by regulating G2/M checkpoint-associated programs and modulating mucin-associated phenotypes, supporting its potential as a risk biomarker and candidate therapeutic target for IGC prevention.
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