lncRNA ZNF667‑AS1 inhibits ovarian cancer progression by interacting with the TNF signaling pathway
Ovarian cancer (OC) is the most lethal gynecological malignancy and poses a significant public health burden. The present study explored the function and mechanism of long noncoding RNA (lncRNA) ZNF667-AS1 in OC progression. The present study conducted a multifaceted evaluation, including transcriptomic analyses, to examine the expression and prognostic value of lncRNA ZNF667-AS1 in OC via the Cancer Genome Atlas and Genotype-Tissue Expression data. <i>In vitro</i> experiments on OC cell lines were used to investigate the functional effect of ZNF667-AS1 via cell proliferation, migration and invasion assays and RNA sequencing and western blotting were used to explore the implicated molecular pathways. ZNF667-AS1 was significantly underexpressed in OC tissues and cell lines. Its expression levels were positively associated with improved patient prognosis and affected both tumor behavior and tumor microenvironment interactions. Functional analysis confirmed the tumor-suppressive role of ZNF667-AS1 and revealed a marked decrease in proliferation, migration and invasion in ZNF667-AS1-overexpressing cells. Additionally, ZNF667-AS1 was identified as a key regulator in the tumor necrosis factor signaling pathway, which suggests a strong link between ZNF667-AS1 expression and OC progression. The present study identified ZNF667-AS1 as a potential biomarker for OC prognosis and treatment and illustrated its significant regulatory effects on the TNF pathway and its broader implications in cancer pathobiology.
Authors
- Fangfang Wu (ORCID: https://orcid.org/0000-0003-4193-4187)
- Tianwen Gao (ORCID: https://orcid.org/0000-0002-8621-8611)
- Xiaoyue Mei
- Tianci Zhang (ORCID: https://orcid.org/0000-0001-9692-1469)
Institutions
- Anhui Medical University (CN)
- Anhui University of Traditional Chinese Medicine (CN)
Publication Details
- Journal
- Experimental and Therapeutic Medicine
- Published
- 2025-03-19
- DOI
- https://doi.org/10.3892/etm.2025.12850
- Citations
- 1
- Primary Topic
- Cancer-related molecular mechanisms research
- Type
- article
- Field-Weighted Citation Impact
- 0.94