ReviewMolecules (Basel, Switzerland)2025
Roles of Post-Translational Modifications of Transcription Factors Involved in Breast Cancer Hypoxia.
Review in Molecules (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed.
- EIF3H Modulates Glycolysis Through LDHA Stabilization in Triple-Negative Breast Cancer.Cancers · 2026Article
- VCPIP1 drives diabetic cardiomyopathy by deubiquitinating AMPKγ1 and preventing AMPKα-γ subunit assembly in cardiomyocytes.Signal transduction and targeted therapy · 2026Article
- Roles of oxygen in the tumorigenesis, progression, and treatment of breast cancer.Medical gas research · 2026Review
- Nuclear-Cytoplasmic Axis in Cancer: From Protein Mislocalization to Anticancer Drug Resistance.Oncology research · 2026Review
- Hypoxic Reprogramming of ACOX1-Driven HSP90AB1 Crotonylation Stabilizes Thioredoxin to Orchestrate Redox Homeostasis in Oral Squamous Cell Carcinoma.Research (Washington, D.C.) · 2026Article
- Multi-omics and experimental validation identify USP54 as a prognostic deubiquitinase promoting pancreatic ductal adenocarcinoma progression within the immune microenvironment.Frontiers in immunology · 2026Article
- The Kv10.1 potassium channel, driver of hypoxia-induced EMT and breast cancer cell aggressiveness.Cancer cell international · 2025Article
- Developments in the study of the role of lactate metabolism in the genesis and progression of thyroid cancer.Frontiers in cell and developmental biology · 2025Review
- Targeting the hypoxia signaling pathway with nanomedicine to reverse immunotherapy resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 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
7 authors.
Funding
Abstract
BC is the most commonly diagnosed cancer and the second leading cause of cancer death among women worldwide. Cellular stress is a condition that leads to disrupted homeostasis by extrinsic and intrinsic factors. Among other stressors, hypoxia is a driving force for breast cancer (BC) progression and a general hallmark of solid tumors. Thus, intratumoral hypoxia is an important determinant of invasion, metastasis, treatment failure, prognosis, and patient mortality. Acquisition of the epithelial-mesenchymal transition (EMT) phenotype is also a consequence of tumor hypoxia. The cellular response to hypoxia is mainly regulated by the hypoxia signaling pathway, governed by hypoxia-inducible factors (HIFs), mainly HIF1α. HIFs are a family of transcription factors (TFs), which induce the expression of target genes involved in cell survival and proliferation, metabolic reprogramming, angiogenesis, resisting apoptosis, invasion, and metastasis. HIF1α cooperates with a large number of other TFs. In this review, we focused on the crosstalk and cooperation between HIF1α and other TFs involved in the cellular response to hypoxia in BC. We identified a cluster of TFs, proposed as the HIF1α-TF interactome, that orchestrates the transcription of target genes involved in hypoxia, due to their post-translational modifications (PTMs), including phosphorylation/dephosphorylation, ubiquitination/deubiquitination, SUMOylation, hydroxylation, acetylation, S-nitrosylation, and palmitoylation. PTMs of these HIF1α-related TFs drive their stability and activity, degradation and turnover, and the bidirectional translocation between the cytoplasm or plasma membrane and nucleus of BC cells, as well as the transcription/activation of proteins encoded by oncogenes or inactivation of tumor suppressor target genes. Consequently, PTMs of TFs in the HIF1α interactome are crucial regulatory mechanisms that drive the cellular response to oxygen deprivation in BC cells.
Indexed as
Identifiers
What 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.