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Contribution of KCTD12 to esophageal squamous cell carcinoma

  • Abbaszadegan, Mohammad Reza1, 2
  • Taghehchian, Negin1, 2
  • Li, Liping3
  • Aarabi, Azadeh1
  • Moghbeli, Meysam4
  • 1 Mashhad University of Medical Sciences, Immunology Research Center, Mashhad, Iran , Mashhad (Iran)
  • 2 Mashhad University of Medical Sciences, Medical Genetics Research Center, Faculty of Medical Sciences, Mashhad, Iran , Mashhad (Iran)
  • 3 The Third Affiliated Hospital of Nanchang University, Department of Clinical Laboratory, Jiangxi, Nanchang, 330008, People’s Republic of China , Jiangxi (China)
  • 4 Mashhad University of Medical Sciences, Department of Modern Sciences and Technologies, Faculty of Medicine, Mashhad, Iran , Mashhad (Iran)
Published Article
BMC Cancer
Springer (Biomed Central Ltd.)
Publication Date
Aug 29, 2018
DOI: 10.1186/s12885-018-4765-z
Springer Nature


BackgroundIt has been shown that the expression of potassium channel tetramerization domain containing 12 (KCTD12) as a regulator of GABAB receptor signaling is reversely associated with gastrointestinal stromal tumors. In present study we examined the probable role of KCTD12 in regulation of several signaling pathways and chromatin remodelers in esophageal squamous cell carcinoma (ESCC).MethodsKCTD12 ectopic expression was done in KYSE30 cell line. Comparative quantitative real time PCR was used to assess the expression of stem cell factors and several factors belonging to the WNT/NOTCH and chromatin remodeling in transfected cells in comparison with non-transfected cells.ResultsWe observed that the KCTD12 significantly down regulated expression of NANOG, SOX2, SALL4, KLF4, MAML1, PYGO2, BMI1, BRG1, MSI1, MEIS1, EGFR, DIDO1, ABCC4, ABCG2, and CRIPTO1 in transfected cells in comparison with non-transfected cells. Migration assay showed a significant decrease in cell movement in ectopic expressed cells in comparison with non-transfected cells (p = 0.02). Moreover, KCTD12 significantly decreased the 5FU resistance in transfected cells (p = 0.01).ConclusionsKCTD12 may exert its inhibitory role in ESCC through the suppression of WNT /NOTCH, stem cell factors, and chromatin remodelers and can be introduced as an efficient therapeutic marker.

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