ArticleClinical, cosmetic and investigational dermatology2024
FOXN3 Regulates Autophagic Activity to Suppress Drug Resistance in Melanoma Cells.
Article in Clinical, cosmetic and investigational dermatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The forkhead box (FOX) family member FOXN3 has been reported to inhibit transcriptional activity associated with regulating tumor development. However, the role of FOXN3 in the pathogenesis of melanoma is not well understood. Objective: To investigate the biological functions of FOXN3 in drug resistance of melanoma. Materials and Methods: The expression of FOXN3 in melanoma was investigated using Gene Expression profiling interactive analysis (GEPIA) and Linkedomics databases. Melanoma cell proliferation, invasion, and migration were assessed using the colony formation assay, the scratch wound healing test, the Transwell invasion assay, and the nude mice xenograft to determine the effects of FOXN3 over-expression and depletion. The functional role of the transcriptional regulator in melanoma cells was tested through chromatin immunoprecipitation, immunofluorescence. Results: FOXN3 was downregulated in melanoma. Over-expression of FOXN3 inhibited the proliferation and motility of melanoma cells, whereas FOXN3 knockdown significantly enhanced the proliferation and motility of melanoma cells. Overexpression of FOXN3 reduced autophagic activity in melanoma cells. Enhanced autophagic activity in drug-resistant melanoma cell lines is related to drug-sensitive cells, and significant differences in FOXN3 localization were observed when comparing melanoma cells that were sensitive and resistant to Vemurafenib. Additionally, FOXN3 has been identified as binding to the promoter region of the cancer antigen Fibrous Sheath Interacting Protein 1 (FSIP1), thereby regulating the expression of this gene. Conclusion: FOXN3 functions as an important regulator of the development and progression of Vemurafenib-resistant melanoma cells, partly owing to its binding to the
Indexed as
Identifiers
What Socratic 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 Socratic graph.