ArticlePloS one2015
Alpha-catulin contributes to drug-resistance of melanoma by activating NF-κB and AP-1.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- The Influence of Dietary Factors on Melanoma Development and Progression: A Comprehensive Review.Nutrients · 2025Review
- Article
- Emerging Roles of the α-Catenin Family Member α-Catulin in Development, Homeostasis and Cancer Progression.International journal of molecular sciences · 2022Review
- Catulin reporter marks a heterogeneous population of invasive breast cancer cells with some demonstrating plasticity and participating in vascular mimicry.Scientific reports · 2022Article
- CTNNAL1 participates in the regulation of mucus overproduction in HDM-induced asthma mouse model through the YAP-ROCK2 pathway.Journal of cellular and molecular medicine · 2022Article
- α-Catulin promotes cancer stemness by antagonizing WWP1-mediated KLF5 degradation in lung cancer.Theranostics · 2022Article
- Catulin Based Reporter System to Track and Characterize the Population of Invasive Cancer Cells in the Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2021Article
- The prediction of survival in Gastric Cancer based on a Robust 13-Gene Signature.Journal of Cancer · 2021Article
- Article
- SPAG9 promotes prostate cancer proliferation and metastasis via MAPK signaling pathway.American journal of translational research · 2019Article
- The elevated activation of NFκB and AP-1 is correlated with differential regulation of Bcl-2 and associated with oral squamous cell carcinoma progression and resistance.Clinical oral investigations · 2017Article
- The identification of molecular target of (20S) ginsenoside Rh2 for its anti-cancer activity.Scientific reports · 2017Article
- Article
- RNA-seq analysis provide new insights into mapk signaling of apolipoproteinciii-induced inflammation in porcine vascular endothelial cells.Cell cycle (Georgetown, Tex.) · 2017Article
- Phenotype-based variation as a biomarker of sensitivity to molecularly targeted therapy in melanoma.MedChemComm · 2017Article
- The upregulated α-catulin expression was involved in head-neck squamous cell carcinogenesis by promoting proliferation, migration, invasion, and epithelial to mesenchymal transition.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Tetrahydroanthraquinone Derivative (±)-4-Deoxyaustrocortilutein Induces Cell Cycle Arrest and Apoptosis in Melanoma Cells via Upregulation of p21 and p53 and Downregulation of NF-kappaB.Journal of Cancer · 2016Article
- Epigenetic mechanisms involved in melanoma pathogenesis and chemoresistance.Annals of translational medicine · 2015Review
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
Melanoma is the most dangerous type of skin cancer accounting for 48,000 deaths worldwide each year and an average survival rate of about 6-10 months with conventional treatment. Tumor metastasis and chemoresistance of melanoma cells are reported as the main reasons for the insufficiency of currently available treatments for late stage melanoma. The cytoskeletal linker protein α-catulin (CTNNAL1) has been shown to be important in inflammation, apoptosis and cytoskeletal reorganization. Recently, we found an elevated expression of α-catulin in melanoma cells. Ectopic expression of α-catulin promoted melanoma progression and occurred concomitantly with the downregulation of E-cadherin and the upregulation of mesenchymal genes such as N-cadherin, Snail/Slug and the matrix metalloproteinases 2 and 9. In the current study we showed that α-catulin knockdown reduced NF-κB and AP-1 activity in malignant melanoma cells. Further, downregulation of α-catulin diminished ERK phosphorylation in malignant melanoma cells and sensitized them to treatment with chemotherapeutic drugs. In particular, cisplatin treatment led to decreased ERK-, JNK- and c-Jun phosphorylation in α-catulin knockdown melanoma cells, which was accompanied by enhanced apoptosis compared to control cells. Altogether, these results suggest that targeted inhibition of α-catulin may be used as a viable therapeutic strategy to chemosensitize melanoma cells to cisplatin by down-regulation of NF-κB and MAPK pathways.
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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.