Abstract 5415: Identifying telomere-related molecular signatures in <i>H. pylori</i> infection and exploring plant-based potential telomerase inhibitors: An <i>in-silico</i> analysis

Abstract International Agency for Cancer Research categorizes Helicobacter pylori as a Class I carcinogen for its known role in gastric cancers, especially among the low-income groups of developing countries where stomach infections are very common. Chronic infection caused by these bacteria results in gastric inflammation that trigger molecular events ultimately leading to cellular transformation. CagA, a pathogenic gene of H. pylori can disrupt multiple molecular targets in human cells and may also interrupt with normal cell proliferation and survival. This study demonstrates the carcinogenic potential of H. pylori by interfering with the function of telomeric complex and contributing to cellular immortality. GEO datasets were used to identify genes that are differentially expressed and how their altered expression compromised the normalcy of shelterin, CST, and TERT-TERC complexes. This study also explores the role of selected proteins that hampers the functioning of double stranded break (DSB) repair at telomeres. Finally, we compare standard and traditional drugs that may interfere with telomerase activity in cancer cells. We found that CagA may trigger the hTERT activation via the AKT-pathway. The target proteins Cdh1 and Pik3ca showed higher binding affinity with phytochemicals then with the standard of care drugs and possible play a role in indirectly inhibiting telomerase. Despite advancements in stomach cancer treatment, the findings from this study attempts to make a useful contribution in understanding H. pylori infection and resultant trigger of cancer hallmarks. Citation Format: Trupti Patel, Ujjayini Chakraborty. Identifying telomere-related molecular signatures in H. pylori infection and exploring plant-based potential telomerase inhibitors: An in-silico analysis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 5415.