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Updated: Jan 8, 2026

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
Characteristics of the immune microenvironment, metabolic microenvironment, and gut microbiota in prostate cancer
Fangmei Xie1, Birong Zhou2, Yinghui Hao1
1Central Laboratory, The Affiliated Panyu Central Hospital of Guangzhou Medical University, Guangzhou, Guangdong, P.R. China.
Abstract:
The tumor microenvironment (TME) is a complex ecosystem comprising tumor cells and their surrounding components, such as stromal cells, extracellular matrix, blood vessels, and signaling molecules. It functions as the "soil" that sustains tumor survival and progression, critically influencing tumor growth, invasion, metastasis, and drug resistance. As a key component of the TME, the tumor immune microenvironment (TIME) refers specifically to the interactive network between tumor cells and the immune system. This interplay dictates whether tumors are recognized and eliminated by immune surveillance or succeed in evading immune detection.The gastrointestinal microecology (GM) system encompasses the gut microbiota and their respective habitats. Gut microbiota influence tumor progression through immune regulation, metabolic modulation, and genotoxic effects, thereby shaping therapeutic responses. Meanwhile, tumor cells employ diverse metabolic pathways to meet heightened bioenergetic and biosynthetic demands and to mitigate oxidative stress-processes essential for their proliferation and survival. These metabolic adaptations significantly shape TME characteristics, including nutrient availability, hypoxia, and the induction of immunosuppression.This review summarizes the roles of the immune microenvironment, metabolic microenvironment, and gut microbiota in the initiation, progression, and treatment of prostate cancer (PCa). It further illustrates how these three components interact to collectively regulate PCa development and therapeutic outcomes. By integrating recent advances in these areas, we aim to provide new insights into the molecular mechanisms of PCa pathogenesis and to inform comprehensive clinical strategies.

