Potential Role of Vaginal Microbiota in Ovarian Cancer Carcinogenesis, Progression and Treatment

Abstract

Ovarian cancer represents one of the most challenging gynecologic cancers which still has numerous unknowns on the underlying pathogenesis. In addition to the verified contributors such as genomic predisposition and medical history in the carcinogenesis, emerging evidence points out the potential role of vaginal microbiota in ovarian cancer. Recent studies have underlined the presence of vaginal microbial dysbiosis in cancer cases. Increasing research also indicates the potential correlations between vaginal microbes and cancer carcinogenesis, progression and treatment. Currently, compared with other gynecologic cancers, reports on the roles of vaginal microbiota in ovarian cancer remain scarce and fragmentary. Therefore, in this review, we summarize the roles of vaginal microbiota in various gynecologic diseases, particularly focusing on the potential mechanisms and possible applications of vaginal microbiota in ovarian cancer, giving insight into the involvement of vaginal microbiota in gynecologic cancer treatment.

Exploring the molecular mechanisms and potential therapeutic strategies of ferroptosis in ovarian cancer

“…The identification of new therapeutic targets or agents is closely linked to the investigation of the molecular mechanism that underlies tumour formation and progression. The cause of ovarian cancer remains unclear, but it is thought to be associated with gonadotropin, genetic factors, inflammation, and other factors [7]. First, existing theory suggests that gonadotrophins and oestrogens act on the ovarian surface epithelium to accumulate DNA damage that eventually leads to malignant transformation [8].…”

Exploring the Relationship between Ovarian Cancer and Genital Microbiota: A Systematic Review and Meta-Analysis

“…While some evidence from the literature has been reported, the available data are not consistent. In the context of OC, this potential relationship is even more debated, as OC etiology can be attributed to multifactorial agents, including genetic predisposition, family history, and hormonal status [16,17].…”

Racial Differences in Vaginal Fluid Metabolites and Association with Systemic Inflammation Markers among Ovarian Cancer Patients: A Pilot Study

“…Additionally, the potential disparate contribution of the vaginal microbiome to inflammatory pathways relevant to ovarian cancer is unclear given that evidence for ovarian cancer is fragmented and scarce relative to other gynecological cancers [19,20]. However, it appears that for ovarian cancer the vaginal microbiome can create a tumor-permissive microenvironment, either directly, or by inducing host immune responses to contribute to cancer-promoting inflammation and cell death avoidance [10,20,21], which in turn drives tumor initiation and progression through increased oxidative stress, DNA damage, and accumulation of mutations [10,22].…”

“…Additionally, the potential disparate contribution of the vaginal microbiome to inflammatory pathways relevant to ovarian cancer is unclear given that evidence for ovarian cancer is fragmented and scarce relative to other gynecological cancers [19,20]. However, it appears that for ovarian cancer the vaginal microbiome can create a tumor-permissive microenvironment, either directly, or by inducing host immune responses to contribute to cancer-promoting inflammation and cell death avoidance [10,20,21], which in turn drives tumor initiation and progression through increased oxidative stress, DNA damage, and accumulation of mutations [10,22]. Pro-carcinogenic metabolites could be upregulated, such as inflammation-inducing lipopolysaccharides, growth-factor-like lysophosphatidic acid [10], and prostaglandins [11], while antineoplastic metabolites could be downregulated through consumption as an energy source for cancer cells, such as tryptophan and indoleproprionic acid [10].…”

“…Pro-carcinogenic metabolites could be upregulated, such as inflammation-inducing lipopolysaccharides, growth-factor-like lysophosphatidic acid [10], and prostaglandins [11], while antineoplastic metabolites could be downregulated through consumption as an energy source for cancer cells, such as tryptophan and indoleproprionic acid [10]. Moreover, the vaginal microbiome can also trigger inflammationinducing signaling pathways involving toll-like receptors that promote a pro-inflammatory response and accelerate tumor growth [20].…”