Endometrial microbiota from endometrial cancer and paired pericancer tissues in postmenopausal women: differences and clinical relevance.

OBJECTIVE: The incidence of postmenopausal endometrial cancer (EC) is rising, and the uterine microbiota has recently been suggested to be an etiology of EC. However, the differences in microbiota profiles in paired EC and the adjacent non-EC endometrium, and the functional microbiota of clinical relevance remain largely unknown. Therefore, we examined the differences in microbiota profiles between EC and non-EC endometrium and investigated their clinical relevance to EC. METHODS: Twenty-eight EC-affected postmenopausal women undergoing hysterectomy were enrolled. Endometrial microbiome from paired EC and adjacent non-EC tissue samples were detected using 16S rRNA sequencing, and the data were analyzed using R language software. RESULTS: The α diversity and evenness of the endometrial bacterial community significantly increased in EC tissues than those in pericancer tissues ( P < 0.05 for all variables). Lactobacillus and Gardnerella were the main bacterial genera present in both EC and adjacent non-EC-invading endometrium, whereas Prevotella , Atopobium , Anaerococcus , Dialister , Porphyromonas , and Peptoniphilus were more commonly enriched in the EC endometrium (corrected P < 0.05 for all variables). Finally, the abundance of some observed endometrial bacteria was associated with clinical aspects, particularly the vaginal pH, vaginal Lactobacillus abundance, and EC clinical stage. CONCLUSIONS: Paired EC and adjacent non-EC endometrium harbor different endometrial microbiota, and the functional bacteria residing in the endometrium are clinically relevant but require further investigation.

LncRNA FENDRR Inhibits ox-LDL Induced Mitochondrial Energy Metabolism Disorder in Aortic Endothelial Cells via miR-18a-5p/PGC-1α Signaling Pathway.

Atherosclerosis (AS) is the main cause of morbidity and mortality in the world. Mitochondrial dysfunction is closely related to AS. At present, several signaling pathways related to mitochondrial dysfunction have been found, one of which is around PGC-1α. PGC-1α is a transcription activator, which is related to mitochondrial biogenesis and antioxidant defense. In this study, we explored the effect of miR-18a-5p/PGC-1α signaling pathway on mitochondrial energy metabolism in HAECs with ox-LDL treatment. The results showed that the mitochondrial energy metabolism disorder in HAECs treated by ox-LDL was related to the downregulation of LncRNA FENDRR and PGC-1α. FENDRR could reverse ox-LDL induced mitochondrial energy metabolism disorder and upregulate the PGC-1α expression. FENDRR could be used as ceRNA to inhibit the miR-18a-5p expression and reduce the negative regulation of miR-18a-5p on PGC-1α. Downregulation of miR-18a-5p expression or upregulation of PGC-1α in ox-LDL treated HAECs could reverse mitochondrial energy metabolism disorder. In conclusion, these findings suggested that FENDRR/miR-18a-5p/PGC-1α signaling pathway regulated mitochondrial energy metabolism in HAECs; ox-LDL downregulated the expression of PGC-1α and cause mitochondrial energy metabolism disorder by inhibiting this signal pathway.