2026-09-21T05:09:42Z https://www.ideals.illinois.edu/oai-pmh

oai:www.ideals.illinois.edu:2142/129288 2025-10-20 col_2142_5131 col_2142_14781 com_2142_5130 com_2142_687 com_2142_397

application/pdf en text Submission original under an indefinite embargo labeled 'Open Access'. The submission was exported from vireo on 2025-10-19 without embargo terms The student, Hehe Zhang, accepted the attached license on 2025-04-30 at 12:26. The student, Hehe Zhang, submitted this Thesis for approval on 2025-04-30 at 12:52. This Thesis was approved for publication on 2025-05-06 at 16:47. DSpace SAF Submission Ingestion Package generated from Vireo submission #22118 on 2025-10-19 at 18:11:23 Elevated colorectal cancer risk in the hnRNP I knockout mice treated with azoxymethane/dextran sulfate sodium Zhang, Hehe 2025-05-06 Pan, Yuan-Xiang Chen, Hong Mei, Wenyan hnRNP I Knockout Mice early-stage tumorigenesis AOM/DSS treatment eng Chronic inflammation and increased epithelial proliferation play an important role in the development of colorectal cancer (CRC), which is one of the most common and lethal cancers worldwide. HnRNP I is an RNA-binding protein that plays an important role in post-transcriptional regulation of gene expression and intestinal barrier function. In this study, hnRNP I knockout (KO) mice of and AOM/DSS chemical induction model were used to investigate the molecular mechanism of hnRNP I deficiency on colon epithelial dysplasia and early carcinogenesis. The results showed that the hnRNP I knockout mice showed significant weight loss and increased disease activity index (DAI) during AOM/DSS treatment. Abnormal crypt foci (ACF) and dysplasia were found in mice. In addition, elevated nuclear β-catenin localization was observed, strongly suggesting Wnt pathway induction. Moreover, the population of goblet cells was significantly decreased, indicating impaired epithelial barrier integrity and heightened mucosal injury. Ki-67 mislocalization indicated abnormal cell proliferation, which was associated with disruption of recess homeostasis. Our results provide strong evidence that loss of hnRNP I lead to a disruption of epithelial proliferation compartmentalization prevents secretory cell differentiation, and drives aberrant Wnt signaling. It indicates a strong correlation between this loss and the direct stimulation of colonic epithelial dysplasia and the initiation of tumors. Collectively, these findings indicate that hnRNP I is an important regulator of intestinal epithelial homeostasis and suppresses tumor development. These findings provide new insights into the molecular mechanisms of inflammation-driven colorectal cancer and establish a theoretical basis for potential intervention approaches that target the hnRNP I regulatory network to inhibit precancerous lesions. 2025-05 Thesis https://hdl.handle.net/2142/129288 Copyright 2025 Hehe Zhang Food Science & Human Nutrition Food Science & Human Nutrition University of Illinois Urbana-Champaign M.S. Thesis