Yin Yang 1 activates JAK-STAT3-mediated epithelial-mesenchymal transition in Helicobacter pylori-induced gastric cancer progression

Sep 28, 2026

BACKGROUND: Helicobacter pylori infection is widely recognized as a major risk factor for gastric cancer through the Correa cascade. Yin Yang 1 (YY1) is a transcription factor with context-dependent roles in cancer progression, but its function in H. pylori-associated inflammatory transformation remains unclear. AIM: Assess YY1 expression in gastric cancer and determine its impact on tumor progression under H. pylori infection. METHODS: Use coculture and infected or xenograft mouse models, measuring YY1, JAK2/STAT3 pathway components, and EMT proteins via Western blot, qRT-PCR, and immunohistochemistry, with survival analysis and functional assays.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages19

Reading Time48 min

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Abstract

Background

Aim

Methods

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Conclusion

| W | J | C | O | World Journal of
Clinical Oncology | | --- | --- | --- | --- | --- | Submit a Manuscript: [https://www.f6publishing.com](https://www.f6publishing.com) World J Clin Oncol 2025 December 24; 16(12): 112626 DOI: 10.5306/wjco.v16.i12.112626 ISSN 2218-4333 (online) ORIGINAL ARTICLE Basic Study Yin Yang 1 activates JAK-STAT3-mediated epithelial-mesenchymal transition in Helicobacter pylori-induced gastric cancer progression Jing-Wan Chen, Jie-Ji Ouyang, Zhen-Hui Wang, Di-Meng Ma, Zhi Zhang, Qiong Teng, Gang Yu, Xiang-Yong Li Specialty type: Oncology Provenance and peer review: Unsolicited article; Externally peer reviewed. Peer-review model: Single blind Peer-review report’s classification Scientific Quality: Grade B, Grade C Novelty: Grade B, Grade C Creativity or Innovation: Grade B, Grade C Scientific Significance: Grade B, Grade C P-Reviewer: Feng KR, PhD, China; Tamizh Selvan G, PhD, Assistant Professor, India Received: August 4, 2025 Revised: September 9, 2025 Accepted: November 13, 2025 Published online: December 24, 2025 Processing time: 143 Days and 23.4 Hours Jing-Wan Chen, Zhen-Hui Wang, Di-Meng Ma, Zhi Zhang, Qiong Teng, Xiang-Yong Li, Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui Province, China Jing-Wan Chen, Jie-Ji Ouyang, Gang Yu, Department of General Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, Anhui Province, China Co-first authors: Jing-Wan Chen and Jie-Ji Ouyang. Co-corresponding authors: Gang Yu and Xiang-Yong Li. Corresponding author: Xiang-Yong Li, PhD, Chief Physician, Professor, Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Shushan District, Hefei 230022, Anhui Province, [China.](China. liyongxiang@ahmu.edu.cn)[ liyongxiang@ahmu.edu.cn](China. liyongxiang@ahmu.edu.cn) Abstract BACKGROUND Helicobacter pylori (H. pylori) infection is widely considered to be a major risk factor for gastric cancer, contributing to its development through the Correa cascade. Yin Yang 1 (YY1) is a transcription factor that acts as a promoter or suppressor of cancer progression. However, the role of YY1 in the inflammatory transformation associated with H. pylori-induced gastric cancer remains unclear. AIM To explore the expression of YY1 in gastric cancer and its impact on cancer progression with H. pylori infection. METHODS H. pylori bacteria were cocultured with GSE1 cells, AGS cells, and SGC7901 cells, as well as in infected and xenograft mouse models. Expression of YY1, members of the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway, and epithelial-mesenchymal transition (EMT)-related proteins in gastric cancer was examined using Western blotting, quantitative realtime polymerase chain reaction, and immunohistochemistry. Survival analysis was performed using the Kaplan-Meier method with the log-rank test. The role of YY1 in gastric cancer cell proliferation was further evaluated through in vitro and in vivo assays. WJCO [https://www.wjgnet.com](https://www.wjgnet.com) 1 December 24, 2025 Volume 16 Issue 12 Chen JW et al. H. pylori promotes gastric oncogenesis through YY1 RESULTS YY1 was highly expressed in gastric cancer tissues and cells. Kaplan-Meier survival curves indicated that high YY1 expression correlated with a poor prognosis. YY1 expression showed a gradually increasing trend in H. pyloriinduced gastritis and gastric tumors. In vivo and in vitro experiments demonstrated that H. pylori infection promoted phosphorylation of JAK2 and STAT3, thereby activating the EMT pathway, in which YY1 played a key role. YY1 and JAK2 interaction was validated by chromatin immunoprecipitation. YY1 knockdown or pharmacological inhibition reversed EMT and suppressed gastric cancer cell proliferation and metastasis. CONCLUSION

FAQs

What is the main aim of the study?

To explore YY1 expression in gastric cancer and determine how YY1 influences cancer progression during Helicobacter pylori infection.

How is YY1 and the JAK2/STAT3-EMT pathway evaluated?

YY1, JAK2/STAT3 signaling components, and EMT-related proteins are measured using Western blotting, qRT-PCR, and immunohistochemistry, with validation of YY1 and JAK2 interaction.

What conclusions are drawn about YY1 in H. pylori-induced gastric cancer?

YY1 contributes importantly to H. pylori-induced gastric cancer progression by activating EMT, and YY1 inhibition reverses malignant phenotypes including proliferation, invasion, and metastasis.

Sep 28, 2026

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