Yingchen Qian

A Crosstalk Analysis of high-risk human papillomavirus, microbiota and vaginal metabolome in cervicovaginal microenvironment

The microbial community has a profound effect on the host microenvironment by altering metabolites. Persistent high-risk human papillomavirus (HRHPV) infection has been implicated as contributors to the initiation and progression of cervical cancer, but the involved mechanisms are unknown. Assessing the metabolic profile of the cervicovaginal microenvironment has the potential to reveal the functional interactions among the host, metabolites and microbes in HRHPV persistence infection and progression to cancer. The vaginal swabs of women were collected and divided into three groups according to the HPV HybridenPture DNA test (HC2). The participants, include 9 who were categorized as HPV-negative, 8 as positive for HPV16, and 9 as positive for HPV18. 16S rRNA gene sequencing and metabolomics analyses were applied to determine the influence of the vaginal microbiota and host metabolism on the link between HPV and cervicovaginal microenvironment. These findings revealed that HRHPV groups have unique metabolic fingerprints that distinguish them from heathy controls. We showed that HRHPV affects changes in microbial metabolic function, which has important implications for the host. Our study further demonstrated metabolite-driven complex host-microbe interactions and assist in understanding the alterations in the HRHPV-induced cervicovaginal microenvironment.

Insulin-induced gene 2 expression is associated with cervical adenocarcinoma malignant behavior

The incidence of cervical adenocarcinoma (CA) as a malignant tumor has increased over the past few decades due to its low detection rate and malignant biological behaviors. Insulin-induced gene 2 (INSIG2), a membrane protein of the endoplasmic reticulum (ER), plays a crucial role in cancer progression. However, there is little known about the connection between INSIG2 and CA. The Human Protein Atlas (HPA) and the Cancer Genome Atlas (TCGA) Cervical Cancer (CESC) data were applied to study the alteration in INSIG2 expression. Biological functions were performed to test the change of malignant behavior. Bioinformatics analysis was conducted to explore the potential affection of INSIG2 in CA progression. Our study confirmed that the high INSIG2 expression levels had a poor prognosis. INSIG2-knockdown inhibited the CA cell proliferation, migration, and invasion of CA cells while downregulating the epithelial-mesenchymal transition (EMT)-associated gene expression levels. Moreover, the enrichment analysis of DEGs showed more potential functions of INSIG2 in the CA progression. We found that INSIG2 knockdown may play a suppressor role in the CA progression, and may provide the potential functional influence in inhibiting of CA development.