Influences of Gastrointestinal Microbiota Dysbiosis on Serum Proinflammatory Markers in Epithelial Ovarian Cancer Development and Progression

Mahoney, Diane E.; Chalise, Prabhakar; Rahman, Faith; Pierce, Janet D.

doi:10.3390/cancers14123022

Cited by 4 publications

(1 citation statement)

References 64 publications

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“…In addition, we demonstrated that GM from patients with EOC showed significant tumor-promoting impacts on EOC model mice, while GM from healthy controls delayed tumor growth and prolonged survival time ( Figure 3 ). This result matched most experimental observations, which showed that GM dysbiosis promotes OC progression by linking it to systemic inflammatory responses 40 , 41 . Chen et al .…”

Section: Discussionsupporting

confidence: 90%

Gut microbiota dysbiosis promotes the development of epithelial ovarian cancer via regulating Hedgehog signaling pathway

et al. 2023

Gut Microbes

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Epithelial ovarian cancer (EOC) is the most lethal gynecological cancer, which remains a threat to female health at all ages. Hypotheses for EOC development include the continuous presence of inflammation, in which microbiota and inflammatory cytokines participate in cancer-related signaling pathway activation. Hedgehog (Hh) signaling is prominent for EOC progression, and interacts with inflammation response related to gut microbiota (GM). However, the precise roles of GM during this process are unknown. Here, we showed that the GM from patients with EOC differed from that of healthy women and had GM dysbiosis. We found that EOC modeling may lead to GM changes in mice, and it restored after the administration of GM from healthy controls, while GM from patients with EOC further exacerbated GM dysbiosis. Furthermore, we found that GM from EOC markedly promoted tumor progression and activated Hh signaling; meanwhile, it increased the extent of inflammation and activated NF-κB signaling, but GM from healthy controls improved them. Our results demonstrate how GM dysbiosis promoted EOC progression by activating Hh signaling mediated by TLR4/NF-κB signaling. We anticipate our assay to be a new thought for exploring the role of GM in EOC development. Furthermore, improving GM dysbiosis is a novel therapeutic approach for delaying EOC development.

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Section: Discussionsupporting

confidence: 90%