Full text
1,884 characters
· extracted from
oa-doi-fallback
· click to expand
Full text loading...
Abstract
Although there is a well-established connection between the gut microbiome and obesity, the specific mechanisms by which microbes regulate cell signaling, inflammation, and adipocyte growth to influence disease severity in obese patients remains largely unclear. Subsequently, while obesity itself is a well-established risk factor for various cancers, the exact mechanisms by which it drives disease progression are not yet definitively known. In this study, we explored the link between obesity-associated microbiome alterations and cancer progression by analyzing microbial abundance in tissue samples from obese and cancer patients, and we identified specific microbes correlated with Body Mass Index (BMI) that are associated with key cancer-related pathways. Notably, BMI-associated microbial species as Pseudomonas fluorescens and Lactobacillus sakei, were linked with both pro-tumor and anti-tumor progression in cancer patients. Additionally, microbes found to be abundant in cancer and obese tissue, such as Pseudomonas baetica, were significantly associated with the upregulation of certain oncogenic signaling pathways. BMI-associated microbes were also correlated with chemokine signaling and TFR2/NFkB-related genes. Both of these have well established roles in inflammatory activity and inflammasome expression, a critical step in obesity related cancer progression. Therefore, these microbes were found to be associated with variations in disease prognosis and patient survival. This study provides new insights into how obesity-related microbiome dysbiosis may be associated with cancer development, and aims to introduce novel potential avenues for precision medicine approaches in cancer treatment.
- Received:
- Version Posted:
Funding
-
University of California, San Diego
(Award RG096651)
- Principal Award Recipient: Not Applicable
Text is read by the "Ask this paper" AI Q&A widget below.
Extraction quality varies by source — PMC NXML preserves structure
cleanly, OA-HTML may include some navigation residue, and OA-PDF can
have broken hyphenation. The publisher copy
(via DOI)
is the canonical version.