ArticleRadiology and oncology2013
p38 MAPK regulates the expression of ether à go-go potassium channel in human osteosarcoma cells.
Article in Radiology and oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- New insights into the physiological, pathological and pharmacological roles of voltage‑gated potassium channel Kv10.1 in cancer (Review).International journal of oncology · 2026Review
- Mechanistic correlation of potassium channel sensing and nitric oxide activity in neuroinflammation.Molecular biology reports · 2025Review
- The p53-mediated cell cycle regulation is a potential mechanism for emodin-suppressing osteosarcoma cells.Heliyon · 2024Article
- Review
- The hEag1 KInternational journal of molecular sciences · 2022Article
- Tanshinone IIA Inhibits Osteosarcoma Growth through a Src Kinase-Dependent Mechanism.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Construction of microRNA-messenger networks for human osteosarcoma.Journal of cellular physiology · 2019Article
- Review
- Eag1 Voltage-Dependent Potassium Channels: Structure, Electrophysiological Characteristics, and Function in Cancer.The Journal of membrane biology · 2017Review
- Kv10.1 K(+) channel: from physiology to cancer.Pflugers Archiv : European journal of physiology · 2016Review
- The Role of KV7.3 in Regulating Osteoblast Maturation and Mineralization.International journal of molecular sciences · 2016Article
- Silencing of hERG1 Gene Inhibits Proliferation and Invasion, and Induces Apoptosis in Human Osteosarcoma Cells by Targeting the NF-κB Pathway.Journal of Cancer · 2016Article
- Prognostic value of some tumor markers in unresectable stage IV oropharyngeal carcinoma patients treated with concomitant radiochemotherapy.Radiology and oncology · 2015Article
- Voltage-gated ion channels in cancer cell proliferation.Cancers · 2015Review
- The prognostic significance of Src and p-Src expression in patients with osteosarcoma.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Differential regulation of human Eag1 channel expression by serum and epidermal growth factor in lung and breast cancer cells.OncoTargets and therapy · 2015Article
- RETRACTED: Silencing of Ether à go-go 1 by shRNA inhibits osteosarcoma growth and cell cycle progression.International journal of molecular sciences · 2014Article
- Potassium channels in cell cycle and cell proliferation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- The roles of K(+) channels in cancer.Nature reviews. Cancer · 2014Review
- MicroRNAs and long non-coding RNAs: prospects in diagnostics and therapy of cancer.Radiology and oncology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe ether à go-go (Eag) channel has been shown to be overexpressed in a variety of cancers. However, the expression and function of Eag in osteosarcoma are poorly understood. In addition, the molecular mechanisms responsible for Eag overexpression in cancer cells remain unclear.
methodsThe expression of Eag in human osteosarcoma cell line MG-63 was detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis. The effect of Eag inhibition on MG-63 cell proliferation was assessed in vitro. The effect of short hairpin RNA (shRNA) mediated knockdown of Eag on osteosarcoma growth was evaluated in xenograft model in vivo. The activation of mitogen-activated protein kinase (MAPK) pathway and p53 in MG-63 cells was detected by Western blot analysis.
resultsEag was overexpressed in MG-63 cells. Imipramine or Eag shRNA significantly suppressed the proliferation of MG-63 cells in vitro and in vivo. MG-63 cell proliferation was specifically inhibited by p38 MAPK inhibitor SB203580 or small interference RNA (siRNA). The inhibition of p38 MAPK activation by SB203580 or siRNA reduced Eag protein level but increased p53 protein level. Moreover, the activation of p53 by nutlin-3 induced cell growth arrest in MG-63 cells and reduced Eag protein level, while the inactivation of p53 by pifithrin-alpha (PFT-α) promoted MG-63 cell growth and increased Eag protein expression.
conclusionsEag channel functions as an oncogene to promote the proliferation of human osteosarocma cells. Furthermore, the high expression of Eag in osteosarcoma cells is regulated by p38 MAPK/p53 pathway.
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.