ArticleCancers2022
FOXC1 Binds Enhancers and Promotes Cisplatin Resistance in Bladder Cancer.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 14 citations in OpenAlex.
- Cisplatin-Resistant Lung Adenocarcinoma Cells Exhibit Increased Proangiogenic Capacity in a Microphysiological Model of Tumor Neovascularization.Cancer medicine · 2026Article
- Cigarette smoke promotes the progression of non-small cell lung cancer by activating ERK1/2-FOXC1 axis to induce epithelial-mesenchymal transition.Cancer cell international · 2026Article
- Review
- hsa-miR-5688 inhibits FOXC1-OCT4/SOX2 feedforward loop that drives chemoresistance in breast cancer stem cells.Molecular therapy. Oncology · 2025Article
- Article
- Molecular Landscape of Bladder Cancer: Key Genes, Transcription Factors, and Drug Interactions.International journal of molecular sciences · 2024Article
- Carcinogenic roles of MAFG-AS1 in human cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- Identifying possible hub genes and biological mechanisms shared between bladder cancer and inflammatory bowel disease using machine learning and integrated bioinformatics.Journal of cancer research and clinical oncology · 2023Article
- Polymorphic renal transporters and cisplatin's toxicity in urinary bladder cancer patients: current perspectives and future directions.Medical oncology (Northwood, London, England) · 2023Review
- The FOXC2 Transcription Factor: A Master Regulator of Chemoresistance in Cancer.Technology in cancer research & treatmentReview
- Identification and validation of a novel prognostic model based on platinum Resistance-related genes in bladder cancer.International braz j urol : official journal of the Brazilian Society of UrologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Chemotherapy resistance is traditionally attributed to DNA mutations that confer a survival advantage under drug selection pressure. However, in bladder cancer and other malignancies, we and others have previously reported that cancer cells can convert spontaneously to an aggressive drug-resistant phenotype without prior drug selection or mutational events. In the current work, we explored possible epigenetic mechanisms behind this phenotypic plasticity. Using Hoechst dye exclusion and flow cytometry, we isolated the aggressive drug-resistant cells and analyzed their chromatin accessibility at regulatory elements. Compared to the rest of the cancer cell population, the aggressive drug-resistant cells exhibited enhancer accessibility changes. In particular, we found that differentially accessible enhancers were enriched for the FOXC1 transcription factor motif, and that FOXC1 was the most significantly overexpressed gene in aggressive drug-resistant cells. ChIP-seq analysis revealed that differentially accessible enhancers in aggressive drug-resistant cells had a higher FOXC1 binding, which regulated the expression of adjacent cancer-relevant genes like
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.