Jingjing Lin

LncRNA SOX9-AS1 promotes the development of endometrial cancer by sponging miR-497-5p and upregulating E2F transcription factor 3

Endometrial cancer (EC) is one of the most prevalent gynecologic malignancies, and long non-coding RNA (lncRNA) SOX9-AS1 has been identified as being upregulated in various cancers, indicating its potential role in driving carcinogenesis. However, the involvement and mechanism of SOX9-AS1 in EC have not been thoroughly investigated. The expression of SOX9-AS1 was assessed using qRT-PCR. The impact of molecular intervention on EC cells was evaluated through cell viability, migration, and invasion assays. Survival probability was analyzed using the Kaplan-Meier method. Bioinformatics predictions, dual-luciferase reporter assays, and rescue experiments were conducted to elucidate the specific competitive endogenous RNA (ceRNA) mechanism of the SOX9-AS1/miR-497-5p/E2F3 axis. SOX9-AS1 expression was significantly upregulated in EC tissues and cells, correlating with poor prognosis in EC patients. Knockdown of SOX9-AS1 inhibited the proliferation, migration, invasion, and glycolysis of EC cells. Mechanistically, miR-497-5p suppressed the proliferation, migration, invasion, and glycolysis of EC by targeting E2F3. Molecular interaction analysis indicate that SOX9-AS1 functions as a molecular sponge for miR-497-5p, thereby increasing E2F3 expression. Our work unveiled a novel mechanism by which SOX9-AS1 promotes EC development, suggesting that targeting the SOX9-AS1/miR-497-5p/E2F3 axis may represent a potential therapeutic strategy for EC.

Correlation analysis between vaginal microecology and high-risk human papillomavirus (HR-HPV)-positive cervical squamous intraepithelial lesions (SIL)

This study is aimed to investigate the correlation between vaginal microecology and high-risk human papillomavirus (HR-HPV)-positive cervical squamous intraepithelial lesions (SIL) using the regression analysis. Patients (n = 372) with HR-HPV-positive from January 2020 to June 2022 were recruited after preliminary confirmation by colposcopy, HPV test, and typing, as well as loop electrosurgical excision procedure. Based on the pathological results, the recruited subjects were divided into 3 groups, that is, negative for intraepithelial lesion or malignancy, low-grade SIL, and high-grade SIL (HSIL). Finally, the clinical factors, virological data, and vaginal microecological changes of the 3 experimental groups were analyzed. Age was identified as a significant risk factor for HSIL, with an OR of 1.048 (95% CI: 1.006–1.094 and P = .026). Various HR-HPV types (HPV16, HPV18, and HPV52) were closely associated with HSIL, with multiple infections significantly increasing the risk (odds ratio, OR: 5.810, P = .04). The changes in the vaginal microecology were strongly associated with HSIL, including elevated pH (>4.5), reduced hydrogen peroxide levels, and increased bacterial vaginosis (BV) prevalence. BV demonstrated a sensitivity of 66.10% and a specificity of 70.31% for predicting HSIL. Furthermore, decreased Lactobacillus levels (OR: 3.20, P < .001) showed their protective role, while elevated sialidase activity (OR: 5.610, P = .002) emerged as a significant risk factor. Accordingly, the key independent predictors for low-grade SIL and HSIL included age, infection type, pH, microbiome density, BV, and sialidase activity. The mixed infection of HPV16, HPV18, HPV52, and HPV resulting in cervical SILs could be closely related to the vaginal microecology.