ArticleBiochemical genetics2025
FNDC1 Facilitates Proliferation, Migration, and Invasion of Breast Cancer Cells Through Modulating Wnt/β-Catenin Pathway.
Article in Biochemical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Review
- Unveiling the multifaceted roles of extracellular vesicles in cancer: insights from molecular imaging and engineering strategies.Acta biochimica et biophysica Sinica · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is the most common malignant cancer and the leading fatal cancer in women around the world. Fibronectin type III domain-containing protein 1 (FNDC1) has been demonstrated to play crucial roles in various tumors. However, the function of FNDC1 in breast cancer remains to be addressed. Increased FNDC1 expression was found in breast cancer that is associated with individual cancer stages and lymph node metastasis through UALCAN analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays indicated that FNDC1 expression was up-regulated in breast cancer cells. The results of Cell Counting Kit-8 and colony formation assays indicated that FNDC1 promoted the proliferation of breast cancer cells. Moreover, FNDC1 knockdown suppressed xenograft tumor growth and inhibited the levels of FNDC1 and marker of proliferation Ki-67. Transwell assay demonstrated that FNDC1 promoted the migration and invasion of breast cancer cells. Importantly, mechanism analysis implied that FNDC1 promoted the Wnt/β-catenin signaling pathway. Notably, Wnt/β-catenin activation with LiCl significantly enhanced the proliferation and epithelial-mesenchymal transformation (EMT) inhibition effect of silencing FNDC1, whereas Wnt/β-catenin inhibition with XAV-939 significantly weakened the proliferation and EMT promotion effect of FNDC1. Analysis of β-catenin expression in the nucleus and cytoplasm showed that FNDC1 promoted β-catenin nuclear translocation. These data suggested that FNDC1 exerts its oncogene function through modulating Wnt/β-catenin signaling pathway. In conclusion, FNDC1 promotes cell proliferation, migration, invasion, and EMT through modulating Wnt/β-catenin signaling pathway in breast cancer, providing a new idea for the development of breast cancer therapeutic targets.
Indexed as
Identifiers
39671143What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.