Yin Yang 1 activates JAK-STAT3-mediated epithelial-mesenchymal transition in -induced gastric cancer progression.
[BACKGROUND] () infection is widely considered to be a major risk factor for gastric cancer, contributing to its development through the Correa cascade.
APA
Chen JW, Ouyang JJ, et al. (2025). Yin Yang 1 activates JAK-STAT3-mediated epithelial-mesenchymal transition in -induced gastric cancer progression.. World journal of clinical oncology, 16(12), 112626. https://doi.org/10.5306/wjco.v16.i12.112626
MLA
Chen JW, et al.. "Yin Yang 1 activates JAK-STAT3-mediated epithelial-mesenchymal transition in -induced gastric cancer progression.." World journal of clinical oncology, vol. 16, no. 12, 2025, pp. 112626.
PMID
41480166
Abstract
[BACKGROUND] () 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 -induced gastric cancer remains unclear.
[AIM] To explore the expression of YY1 in gastric cancer and its impact on cancer progression with infection.
[METHODS] 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 real-time 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 and assays.
[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 -induced gastritis and gastric tumors. and experiments demonstrated that 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] These results suggest that YY1 plays an important role in progression of -induced gastric cancer by activating EMT.
[AIM] To explore the expression of YY1 in gastric cancer and its impact on cancer progression with infection.
[METHODS] 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 real-time 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 and assays.
[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 -induced gastritis and gastric tumors. and experiments demonstrated that 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] These results suggest that YY1 plays an important role in progression of -induced gastric cancer by activating EMT.