ArticleThe Journal of biological chemistry2012
Regulation of sodium iodide symporter gene expression by Rac1/p38β mitogen-activated protein kinase signaling pathway in MCF-7 breast cancer cells.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Therapeutic Potential of Sodium Selenite Application for Promoting Radioactive Iodine Avidity in Papillary Thyroid Cancer.Bioinorganic chemistry and applications · 2026Article
- Rac1 activation in oral squamous cell carcinoma as a predictive factor associated with lymph node metastasis.International journal of clinical oncology · 2023Article
- Article
- Review
- Epidermal Growth Factor and Adenosine Triphosphate Induce Natrium Iodide Symporter Expression in Breast Cancer Cell Lines.Open access Macedonian journal of medical sciences · 2019Article
- The correlation between breast cancer and urinary iodine excretion levels.The Journal of international medical research · 2018Article
- Prognostic and Clinicopathological Value of Rac1 in Cancer Survival: Evidence from a Meta-Analysis.Journal of Cancer · 2018Review
- GLIS3 is indispensable for TSH/TSHR-dependent thyroid hormone biosynthesis and follicular cell proliferation.The Journal of clinical investigation · 2017Article
- Sodium iodide symporter (NIS) in extrathyroidal malignancies: focus on breast and urological cancer.BMC cancer · 2014Review
- The sodium/iodide symporter NIS is a transcriptional target of the p53-family members in liver cancer cells.Cell death & disease · 2013Article
- MEK inhibition leads to lysosome-mediated Na+/I- symporter protein degradation in human breast cancer cells.Endocrine-related cancer · 2013Article
- The tyrosine kinase c-Met contributes to the pro-tumorigenic function of the p38 kinase in human bile duct cholangiocarcinoma cells.The Journal of biological chemistry · 2012Article
- The sodium iodide symporter (NIS): regulation and approaches to targeting for cancer therapeutics.Pharmacology & therapeutics · 2012Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Activation of p38 MAPK is a key pathway for cell proliferation and differentiation in breast cancer and thyroid cells. The sodium/iodide symporter (NIS) concentrates iodide in the thyroid and lactating breast. All-trans-retinoic acid (tRA) markedly induces NIS activity in some breast cancer cell lines and promotes uptake of β-emitting radioiodide (131)I sufficient for targeted cytotoxicity. To identify a signal transduction pathway that selectively stimulates NIS expression, we investigated regulation by the Rac1-p38 signaling pathway in MCF-7 breast cancer cells and compared it with regulation in FRTL-5 rat thyroid cells. Loss of function experiments with pharmacologic inhibitors and small interfering RNA, as well as RT-PCR analysis of p38 isoforms, demonstrated the requirement of Rac1, MAPK kinase 3B, and p38β for the full expression of NIS in MCF-7 cells. In contrast, p38α was critical for NIS expression in FRTL-5 cells. Treatment with tRA or overexpression of Rac1 induced the phosphorylation of p38 isoforms, including p38β. A dominant negative mutant of Rac1 abolished tRA-induced phosphorylation in MCF-7 cells. Overexpression of p38β or Rac1 significantly enhanced (1.9- and 3.9-fold, respectively), the tRA-stimulated NIS expression in MCF-7 cells. This study demonstrates differential regulation of NIS by distinct p38 isoforms in breast cancer cells and thyroid cells. Targeting isoform-selective activation of p38 may enhance NIS induction, resulting in higher efficacy of (131)I concentration and treatment of breast cancer.
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