The role and mechanism of hepatocyte nuclear factor 1β in the occurrence and development of different human tumors: A pan-cancer analysis.

Abstract

Carcinomatosis is one of the leading threats to human public fitness. HNF1B is a critical transcription element in vertebrate proliferation and oncogenesis, which has been shown to play roles in reactive oxygen species (ROS) metabolism. Our previous results have identified HNF1B as a tumor suppressor that could inhibit the malignant progression of prostate cancer. Yet there is no pan-carcinomatosis analysis of HNF1B, which could help us better understand common and unique underlying mechanisms in mankind knubs to enhance novel and competent treatment. Here, in our research, we evaluated the utterance pattern and explored the function of HNF1B in 33 knub categories using the data from the Cancer Genome Atlas Program (TCGA), Gene Expression Omnibus (GEO), and CLNICAL PROTEOMICTUMOR ANALYSIS CONSORTIUM (CPTAC) dataset. We found different HNF1B roles in various cancer types. HNF1B was upregulated in CHOL, STAD, KIRP, and THCA, and was downregulated in GBM, KICH, COAD, KIRC, LUSC, SARC, PAAD, and TGCT. Prognostic analyses indicated that higher HNF1B displayed better illness outcomes in BLCA, READ, and PRAD, while poorer outcomes in LUSC and THYM. HNF1B mutation was most frequent in endometrial cancer but was not associated with disease prognosis. It was discovered that HNF1B utterance relevant to endothelial cell penetration status in BLCA, ESCA, LUAD, LUSC, and TGCT, and carcinomatosis-associated fibroblast infiltration was observed in ESCA, KIRC, LIHC, and TGCT. Moreover, functional enrichment analysis disclosed that metabolism-related functions were implicated in the function of HNF1B. Taken together, our pan- carcinomatosis analysis showed the complicated roles of HNF1B in a variety of carcinomatoses, being able to improve the extensive comprehension of HNF1B's role in tumorigenesis.