Hongmei Wang

Disfunction of communication among immune cells in minimal-deviation adenocarcinoma of the cervix as an immunotherapeutic opportunity

Minimal deviation adenocarcinoma (MDA) of the uterine cervix, also referred to as malignant adenoma, is a rare subtype of cervical adenocarcinoma that exhibits histological characteristics resembling those of benign tumors, resulting in a low diagnostic rate and a lack of effective treatment options. The transcriptomic features of MDA at the single-cell resolution and within the tumor microenvironment (TME) remain unclear. In this study, we conducted single-cell transcriptomic analyses of MDA samples (Ca) and adjacent normal tissues (PCa). The present study reveals the prevalence of dendritic cells (DCs) and T cells in the carcinoma (Ca) of mammary ductal adenocarcinoma (MDA), with DCs undergoing significant metabolic reprogramming and immune stress. Additionally, our findings demonstrate the crucial involvement of DCs and T cells in the pathogenesis and metastatic progression of MDA, as evidenced by single-cell transcriptomic profiling of MDA and HPV samples. This resource provides a more profound understanding of the indolent nature of MDA and may prove useful in the development of MDA immunotherapy.

PTPN2 acts as a tumor suppressor and therapeutic target in ovarian cancer

Ovarian cancer (OC) remains the most lethal gynecological malignancy, with metastasis and chemoresistance driving poor outcomes. Non-receptor protein tyrosine phosphatase 2 (PTPN2) is a critical regulator of oncogenic signaling pathways, but its role in OC progression remains poorly understood. Here, we identify PTPN2 as a critical tumor suppressor in OC through integrated bioinformatics and functional studies. Bioinformatics analysis revealed significant PTPN2 downregulation in OC tissues, correlating with advanced tumor stage and poor patient survival. Experimental validation confirmed reduced PTPN2 expression at both mRNA and protein levels in clinical specimens. Functional studies demonstrated that PTPN2 overexpression inhibits OC cell proliferation, migration, and motility. Mechanistically, PTPN2 maintains epithelial cell characteristics by upregulating E-cadherin while suppressing mesenchymal markers Snail and Twist through negative regulation of ERK1/2 phosphorylation. Our findings not only expand the current understanding of PTPN2's role in cancer biology but also suggest its dual potential as both a prognostic biomarker and a promising therapeutic target for OC treatment.