ArticleFrontiers in oncology2025
PMAIP1 regulates the progression of follicular thyroid carcinoma through the Wnt3/FOSL1 pathway.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Integrated single-cell and machine learning analysis identifies PMAIP1 as a novel biomarker for predicting prognosis and immunotherapy response in colorectal cancer.Scientific reports · 2025Article
- The Epithelial Cell-Associated Gene PMAIP1 Serves as a Prognostic Biomarker for Lung Adenocarcinoma and Can Regulate the Stemness of Lung Cancer.Stem cells international · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: In thyroid carcinoma (TC), follicular thyroid carcinoma (FTC) represents the second most prevalent pathological type following papillary thyroid carcinoma. Notably, FTC exhibits a more aggressive clinical course and a higher propensity for distant metastasis. However, the underlying mechanisms governing the progression of FTC remain poorly understood. PMAIP1 is a gene implicated in various cancers and biological processes. Investigating the role and mechanism of PMAIP1 in FTC is crucial for enhancing our understanding of FTC and informing clinical treatment strategies. Methods: This study examined the expression level of PMAIP1 in FTC through comprehensive analysis of databases, tumor tissues, and cell lines. Following the establishment of a stably transfected plasmid in cell lines, a series of functional assays and subcutaneous xenograft experiment were conducted to investigate the role of PMAIP1 in FTC. Additionally, transcriptome sequencing was employed to identify potential signaling pathways associated with PMAIP1. Mechanistic studies involved a series of rescue experiments to elucidate the regulatory mechanisms of PMAIP1 in FTC. Results: PMAIP1 was found to be highly expressed in FTC, and its knockdown significantly inhibited the proliferation and metastasis of FTC cells both Discussion: In conclusion, our research demonstrated that PMAIP1 emerges as a novel pro-cancer factor in FTC, and its knockdown significantly inhibited the proliferation and metastasis of FTC both
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