ArticleCell death & disease2016
The Fra-1-miR-134-SDS22 feedback loop amplifies ERK/JNK signaling and reduces chemosensitivity in ovarian cancer cells.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 59 citations in OpenAlex.
- Review
- The AP-1 factor JUNB correlates with poor survival of patients with esophageal adenocarcinoma.Scientific reports · 2025Article
- FOSL1 transcriptionally dictates the Warburg effect and enhances chemoresistance in triple-negative breast cancer.Journal of translational medicine · 2025Article
- RNA Sequencing Identifies Novel Signaling Pathways and Potential Drug Target Genes Induced by FOSL1 in Glioma Progression and Stemness.Biologics : targets & therapy · 2025Article
- Noncoding RNAs as regulators of FOSL1 in cancer.Frontiers in immunology · 2025Review
- Mechanisms of the JNK/p38 MAPK signaling pathway in drug resistance in ovarian cancer.Frontiers in oncology · 2025Review
- FOSL1 is a key regulator of a super-enhancer driving TCOF1 expression in triple-negative breast cancer.Epigenetics & chromatin · 2024Article
- Interaction of NF-κB and FOSL1 drives glioma stemness.Cellular and molecular life sciences : CMLS · 2024Article
- FOSL1's Oncogene Roles in Glioma/Glioma Stem Cells and Tumorigenesis: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Article
- Fra-1 affects chemotherapy sensitivity by inhibiting ferroptosis in gastric cancer cells.Cancer drug resistance (Alhambra, Calif.) · 2024Article
- TRPM7 transactivates the FOSL1 gene through STAT3 and enhances glioma stemness.Cellular and molecular life sciences : CMLS · 2023Article
- Multiple Fra-1-bound enhancers showing different molecular and functional features can cooperate to repress gene transcription.Cell & bioscience · 2023Article
- Article
- ERK inhibitor ASN007 effectively overcomes acquired resistance to EGFR inhibitor in non-small cell lung cancer.Investigational new drugs · 2022Article
- The Fra-1/AP-1 Oncoprotein: From the "Undruggable" Transcription Factor to Therapeutic Targeting.Cancers · 2022Review
- MiR-137 regulates low-intensity shear stress-induced human aortic endothelial cell apoptosis via JNK/AP-1 signaling.Journal of physiology and biochemistry · 2021Article
- Current Implications of microRNAs in Genome Stability and Stress Responses of Ovarian Cancer.Cancers · 2021Review
- Matrine inhibits ovarian cancer cell viability and promotes apoptosis by regulating the ERK/JNK signaling pathway via p38MAPK.Oncology reports · 2021Article
- The nuclear oncoprotein Fra-1: a transcription factor knocking on therapeutic applications' door.Oncogene · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Fra-1 transcription factor is frequently upregulated in multiple types of tumors. Here we found that Fra-1 promotes miR-134 expression. miR-134 activates JNK and ERK by targeting SDS22, which in turn induces Fra-1 expression and leads to miR-134 upregulation. In addition, miR-134 augmented H2AX S139 phosphorylation by activating JNK and promoted non-homologous end joining (NHEJ)-mediated DNA repair. Therefore, ectopic miR-134 expression reduced chemosensitivity in ovarian cancer cells. Furthermore, miR-134 promotes cell proliferation, migration and invasion of ovarian cancer cells, and enhances tumor growth in vivo. Of particular significance, both Fra-1 and miR-134 are upregulated in ovarian cancer tissues, and Fra-1 and miR-134 expression is positively correlated. High levels of miR-134 expression were associated with a reduced median survival of ovarian cancer patients. Our study revealed that a Fra-1-miR-134 axis drives a positive feedback loop that amplifies ERK/JNK signaling and reduces chemosensitivity in ovarian cancer 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.