A reinvestigation of somatic hypermethylation at the PTEN CpG island in cancer cell lines

Hesson, Luke B., Packham, Deborah, Pontzer, Emily, Funchain, Pauline, Eng, Charis and Ward, Robyn L. (2012) A reinvestigation of somatic hypermethylation at the PTEN CpG island in cancer cell lines. Biological Procedures Online, 14 5: . doi:10.1186/1480-9222-14-5


Author Hesson, Luke B.
Packham, Deborah
Pontzer, Emily
Funchain, Pauline
Eng, Charis
Ward, Robyn L.
Title A reinvestigation of somatic hypermethylation at the PTEN CpG island in cancer cell lines
Journal name Biological Procedures Online   Check publisher's open access policy
ISSN 1480-9222
Publication date 2012
Year available 2012
Sub-type Article (original research)
DOI 10.1186/1480-9222-14-5
Open Access Status DOI
Volume 14
Issue 5
Total pages 8
Place of publication London, United Kingdom
Publisher BioMed Central
Collection year 2012
Language eng
Formatted abstract
Background: PTEN is an important tumour suppressor gene that is mutated in Cowden syndrome as well as
various sporadic cancers. CpG island hypermethylation is another route to tumour suppressor gene inactivation,
however, the literature regarding PTEN hypermethylation in cancer is controversial. Furthermore, investigation of
the methylation status of the PTEN CpG island is challenging due to sequence homology with the PTEN
pseudogene, PTENP1. PTEN shares a CpG island promoter with another gene known as KLLN. Here we present a
thorough reinvestigation of the methylation status of the PTEN CpG island in DNA from colorectal, breast, ovarian,
glioma, lung and haematological cancer cell lines.

Results: Using a range of bisulphite-based PCR assays we investigated 6 regions across the PTEN CpG island. We
found that regions 1-4 were not methylated in cancer cell lines (0/36). By allelic bisulphite sequencing and
pyrosequencing methylation was detected in regions 5 and 6 in colorectal, breast and haematological cancer cell
lines. However, methylation detected in this region was associated with the PTENP1 promoter and not the PTEN
CpG island.

Conclusions: We show that methylation of the PTEN CpG island is a rare event in cancer cell lines and that
apparent methylation most likely originates from homologous regions of the PTENP1 pseudogene promoter. Future
studies should utilize assays that reliably discriminate between PTEN and PTENP1 to avoid data misinterpretation
Keyword Cowden syndrome
Dna methylation
Epigenetic
Killin
Pseudogene
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Office of the Vice-Chancellor
 
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Created: Tue, 10 Feb 2015, 13:25:08 EST by Ms Kate Rowe on behalf of Office of Deputy Vice-Chancellor (Research)