ArticleOncogene2004
p38 MAP kinase signaling is necessary for rat chondrosarcoma cell proliferation.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 53 citations in OpenAlex.
- TRPV6 as A Target for Cancer Therapy.Journal of Cancer · 2020Review
- p38 differentially regulates ERK, p21, and mitogenic signalling in two pancreatic carcinoma cell lines.Journal of cell communication and signaling · 2018Article
- Article
- hMAGEA2 promotes progression of breast cancer by regulating Akt and Erk1/2 pathways.Oncotarget · 2017Article
- Power Frequency Magnetic Fields Affect the p38 MAPK-Mediated Regulation of NB69 Cell Proliferation Implication of Free Radicals.International journal of molecular sciences · 2016Article
- Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy.Oxidative medicine and cellular longevity · 2016Review
- p38α MAPK pathway: a key factor in colorectal cancer therapy and chemoresistance.World journal of gastroenterology · 2014Review
- Genetic alterations in chondrosarcomas - keys to targeted therapies?Cellular oncology (Dordrecht, Netherlands) · 2014Review
- Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts.Cell communication and signaling : CCS · 2012Article
- Correlation between p38 mitogen-activated protein kinase and human telomerase reverse transcriptase in sarcomas.Journal of experimental & clinical cancer research : CR · 2012Article
- Modeling the transcriptional consequences of epidermal growth factor receptor ablation in Ras-initiated squamous cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Human p38 mitogen-activated protein kinase inhibitor drugs inhibit Plasmodium falciparum replication.Experimental parasitology · 2011Article
- Signal integration by JNK and p38 MAPK pathways in cancer development.Nature reviews. Cancer · 2009Review
- Src kinase inhibition promotes the chondrocyte phenotype.Arthritis research & therapy · 2007Article
- The transcription factor ATF3 is upregulated during chondrocyte differentiation and represses cyclin D1 and A gene transcription.BMC molecular biology · 2006Article
- Activation of MEK/ERK and PI3K/Akt pathways by fibronectin requires integrin alphav-mediated ADAM activity in hepatocellular carcinoma: a novel functional target for gefitinib.Cancer science · 2006Article
- Constitutive activation of MKK6 in chondrocytes of transgenic mice inhibits proliferation and delays endochondral bone formation.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chondrosarcomas represent the second most frequent class of primary skeletal malignancies. This tumor type is highly resistant to radiation therapy and currently available chemotherapies, thereby limiting treatment choice to surgical resection. Identifying the mechanisms responsible for chondrosarcoma cell proliferation is therefore crucial for the development of new treatment strategies. Here, we demonstrate a significant reduction in rat chondrosarcoma cell proliferation following treatment with pharmacological inhibitors (SB202190 and PD169316) of p38 mitogen-activated protein (MAP) kinases. In an attempt to dissect possible mechanisms, we investigated the effect of p38 inhibition on promoter activity of cell-cycle genes. Surprisingly, p38 inhibition resulted in upregulation of the activities of all three D-type cyclin promoters. In addition, p38 inhibitors induced increased transcription of the cell-cycle inhibitor p21(waf1/cip1). As expected, promoter activity of the cyclin A gene, which lies downstream of D-type cyclins and p21 in cell-cycle progression, was strongly reduced by p38 inhibitors. These effects were independent of a cyclic AMP response element and conferred by the proximal 150 nucleotides of the cyclin A promoter. Decreased transcription was accompanied by greatly reduced cyclin A protein levels upon p38 inhibition. These observations indicate complex regulation of chondrosarcoma cell-cycle progression by p38 signaling, and suggest that components of p38 MAP kinase pathways may be effective targets in the treatment of these tumors.
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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.