Next Article in Journal
FBXW7 in Cancer: What Has Been Unraveled Thus Far?
Previous Article in Journal
Mouse-Derived Isograft (MDI) In Vivo Tumor Models I. Spontaneous sMDI Models: Characterization and Cancer Therapeutic Approaches
Article Menu
Issue 2 (February) cover image

Export Article

Open AccessArticle
Cancers 2019, 11(2), 245; https://doi.org/10.3390/cancers11020245

KCNMA1 Expression Is Downregulated in Colorectal Cancer via Epigenetic Mechanisms

1
Department of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 89, 95123 Catania, Italy
2
IRCCS Centro Neurolesi “Bonino-Pulejo”, Strada Statale 113, C.da Casazza, 98124 Messina, Italy
3
Department of Medical and Surgical Sciences and Advanced Technology “G.F. Ingrassia”, University of Catania, Via Santa Sofia 86, 95123 Catania, Italy
*
Author to whom correspondence should be addressed.
Received: 17 December 2018 / Revised: 14 February 2019 / Accepted: 16 February 2019 / Published: 19 February 2019
  |  
PDF [3566 KB, uploaded 21 February 2019]
  |  

Abstract

KCNMA1 is a gene located at 10q22 that encodes the pore-forming α-subunit of the large-conductance Ca2+-activated K+ channel. KCNMA1 is down-regulated in gastric carcinoma tumors, through hypermethylation of its promoter. In the present study, we have evaluated the expression levels of KCNMA1 both in a mouse model of Colorectal Cancer (CRC) and in human CRC samples. Additionally, epigenetic mechanisms of KCNMA1 gene regulation were investigated. We observed a significant down-regulation of KCNMA1 both in a human and mouse model of CRC. No differences in KCNMA1 levels were, however, observed at different TNM stages. We also wanted to determine whether the modulation in KCNMA1 was dependent on epigenetic mechanisms. A statistically significant inverse correlation between KCNMA1 expression and mir-17-5p levels was observed in patients with CRC. Furthermore, in the tumor samples, we found a significant hypermethylation of the promoter, in the loci cg24113782 and cg25655799, compared to healthy tissue. Overall, our data suggest the possible use of KCNMA1 as a therapeutic target in the early stages of CRC. View Full-Text
Keywords: KCNMA1; Colorectal Cancer; epigenetics; DNA methylation; mir-17-5p; mir-31; mir-211 KCNMA1; Colorectal Cancer; epigenetics; DNA methylation; mir-17-5p; mir-31; mir-211
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Basile, M.S.; Fagone, P.; Mangano, K.; Mammana, S.; Magro, G.; Salvatorelli, L.; Li Destri, G.; La Greca, G.; Nicoletti, F.; Puleo, S.; Pesce, A. KCNMA1 Expression Is Downregulated in Colorectal Cancer via Epigenetic Mechanisms. Cancers 2019, 11, 245.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Cancers EISSN 2072-6694 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top