Page 44 - JCTR-11-5

Journal of Clinical and
Translational Research Vaginal microbiota in menopause pathologies

as a preventive and therapeutic option for urinary and with its repair, thereby increasing mutation risk. This may
pelvic floor disorders. lead to the activation of molecules such as nuclear factor
kappa-light-chain-enhancer of activated B cells (NF-κB),
10. Vaginal and urinary microbiota in which suppress programmed cell death and stimulate
menopause and gynecological cancer blood vessel formation, both of which are critical to tumor

The female reproductive tract contains a specialized progression. Moreover, microbial metabolites from the
microbiome crucial for maintaining health, especially gut, including deoxycholic acid and lipoteichoic acid, can
in the lower tract, where Lactobacillus species dominate circulate through the body and contribute to the emergence
26,59,60
during the reproductive years. These bacteria interact of cancers in distant organs, such as the liver.
beneficially with the host, preserving vaginal balance. Various pathogenic bacteria are linked to carcinogenesis.
When this harmony is disrupted, known as dysbiosis, For example, Helicobacter pylori is associated with gastric
61
it can impair immune and metabolic pathways, leading cancer, while Fusobacterium nucleatum has been linked
62
to processes associated with malignancy, such as to colon cancer. Research in animal models has shown
persistent inflammation, genomic instability, and altered that reducing the microbiota through antibiotics decreases
metabolism. 56-58 These disruptions may contribute to the tumor formation in organs such as the colon and liver,
onset and progression of gynecologic cancers, including suggesting that a dysbiotic microbiota may promote tumor
cervical, ovarian, and endometrial cancers, potentially development. 26
through both indirect and direct mechanisms. While Alterations in microbial balance have also been
56
the involvement of specific bacterial pathogens in these associated with the initiation and development of tumors
cancers remains uncertain, broad shifts in microbial in other parts of the body, including the skin, mouth,
26
composition have been linked to tumorigenesis. Multiple respiratory system, and reproductive tract. Dysbiotic
risk factors are implicated in these cancers, including STIs microorganisms can cause failures in the epithelial
(human papillomavirus [HPV], C. trachomatis, HIV), use barrier, immune dysregulation, and genotoxicity, creating
of postmenopausal hormones, obesity, tobacco use, and a microenvironment conducive to cancer. Chronic
inherited genetic predispositions. More recently, research inflammation is one of the best-documented mechanisms
has started exploring how human-associated microbial modulating cancer characteristics. For instance,
communities might influence cancer development in the F. nucleatum in colorectal cancer activates the NF-κB
reproductive tract. Although it is still unclear whether pathway, promoting the production of inflammatory
microbial alterations are a driving factor or a byproduct cytokines such as IL-6 and TNF, which in turn promote cell
of these malignancies, increasing data support the notion proliferation and angiogenesis, both of which are essential
that the microbiota may foster tumorigenesis through characteristics of cancer. 56
mechanisms such as reduced apoptosis, enhanced cell
proliferation, and genomic instability. 26,57 C. trachomatis has been identified as one of the
bacteria involved in the development of gynecologic
The urogenital microbiota, influenced by factors cancers. It facilitates tumor initiation by triggering
such as sex and age, also plays an important role in epithelial-mesenchymal transition, which reduces cell
gynecological carcinogenesis. In women with low estrogen adhesion and disrupts mechanisms that repair DNA
levels, such as those before puberty or postmenopausal, a damage. In addition, the interplay between the gut and
63
mixture of anaerobic bacteria predominates, potentially VM can modulate estrogen concentrations, influencing
creating a less protective environment against infections hormone-dependent disorders like endometriosis and
and cellular alterations. In contrast, during pregnancy specific cancers. The estrobolome, comprising microbial
or in young women with high estrogen levels, the VM genes responsible for estrogen metabolism, controls
remains more stable and is dominated by Lactobacillus, circulating estrogen levels via β-glucuronidase activity.
which protects the reproductive tract against pathogens Dysbiosis can interfere with this regulation, leading to
and reduces the risk of gynecological cancers. Harmful hormonal imbalances that may contribute to gynecologic
56
bacteria significantly contribute to the weakening of the conditions. Beyond its impact on cancer development,
64
epithelial barrier by producing hydrolytic enzymes and the microbiota also plays a role in treatment outcomes
promoting the release of proinflammatory cytokines like among women with gynecologic malignancies. Anticancer
IL-6 and TNF. These actions drive chronic inflammation strategies, including chemotherapy and radiotherapy,
58
and disturb local metabolic processes, creating conditions can disrupt microbial communities, potentially affecting
that may support carcinogenesis. They also induce genetic treatment effectiveness and side effects. Interventions
instability by either damaging DNA directly or interfering such as probiotics or fecal microbiota transplantation

Volume 11 Issue 5 (2025) 38 doi: 10.36922/JCTR025150016