Peptostreptococcus anaerobius promotes cervical cancer angiogenesis by upregulating SCD to activate ERK pathway

Accumulating evidence indicates that virginal microbiota dysbiosis is a distinct feature of cervical cancer. As cervical lesions progress towards malignancy, the dominance of <i>Lactobacillus</i> species within the vaginal microbiota is progressively replaced by anaerobic bacteria, with <i>Peptostreptococcus anaerobius</i> (<i>P. anaerobius</i>) being a noticeable one. Despite this well-documented microbial shift, the precise functional role of <i>P. anaerobius</i> in cervical cancer development and progression has remained unclear. Our study demonstrated that <i>P. anaerobius</i> promoted cervical cancer cells proliferation and enhanced tube formation of human umbilical vein endothelial cells (HUVECs). Furthermore, we identified a significant upregulation of stearoyl-CoA desaturase 1 (SCD) following the introduction of <i>P. anaerobius</i>, leading to subsequent activation of the extracellular signal-regulated kinase (ERK) signaling pathway. Moreover, supplement with <i>P. anaerobius</i> failed to reverse the ERK1/2 inhibitor-induced suppression of the tube-formation. <i>In vivo</i> validation revealed that <i>P. anaerobius</i> exerted its influence on angiogenesis by regulating SCD expression and ERK pathway acvivation. Collectively, these findings reveal an oncogenic role of <i>P. anaerobius</i> in cervical cancer, mediated by the SCD-ERK signaling axis to drive angiogenesis. This work provides novel mechanistic insights into the contribution of vaginal microbiota to gynecologic malignancies.