Inactivation of the PTEN gene by mutation, exonic deletion, and loss of transcript in human oral squamous cell carcinomas

Shin, Kihyuk; Kim, Jin Man; Rho, Kyong Su; Park, Kyung-Bee; Oh, Joo Hyun; Min, Byoung-Goo

doi:10.3892/ijo.21.5.997

Cited by 22 publications

(23 citation statements)

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“…Squarize et al evaluated the expression of PTEN by immunohistochemistal analysis in OSCC and concluded that aggressive tumors with a high malignancy did not express PTEN, and that PTEN is related to the histology and behavior of OSCC and may therefore be used as a prognostic marker (17). Shin et al demonstrated that the inactivation of PTEN by either mutation or loss of transcription is related to the pathogenesis of some oral cancers (18). These findings are comparable to our results.…”

Section: Discussionsupporting

confidence: 82%

PTEN expression and methylation status in oral squamous cell carcinoma

Kurasawa

Shiiba²,

Nakamura³

et al. 2008

Oncol Rep

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Abstract. PTEN is a tumor suppressor gene located on chromosome10q23.3. In addition to genetic mutations and deletions, the down-regulation of PTEN has been found in various malignant tumors. However, little is known about the profile of PTEN gene in oral carcinomas. In this study, the expression profiles and genetic alterations of PTEN were examined in 113 oral squamous cell carcinoma (OSCC) cases and 9 OSCC-derived cell lines. An immunohistochemical analysis showed statistically significant differences in the immunohistochemical (IHC) scores for PTEN protein in normal tissues and in cancerous regions (P=0.0104), suggesting that PTEN protein expression is down-regulated in OSCC. No significant correlations existed between the down-regulation of PTEN protein expression and the clinicopathological features of the tumor. Reverse transcriptionpolymerase chain reaction (RT-PCR) analysis showed a lower PTEN mRNA expression in the 9 OSCC-derived cell lines examined, as compared to the normal oral epithelium cells. However, treatment with a demethylating reagent restored PTEN mRNA expression in 4 cell lines. No genetic mutations were detected in these cell lines by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis. The results suggest that epigenetic changes may be related to the down-regulation of PTEN expression. We therefore conclude that PTEN is a crucial molecule in the tumorigenesis of OSCC.

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Section: Discussionsupporting

confidence: 82%

PTEN expression and methylation status in oral squamous cell carcinoma

Kurasawa

Shiiba²,

Nakamura³

et al. 2008

Oncol Rep

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“…However, deletions or point mutations are unlikely to play a key role in OSCC tumorigenesis (44). Shin et al (45) reported that the contribution of PTEN inactivation by either mutation or loss of transcript to the pathogenesis of Korean oral cancer was low. Furthermore, Ishida et al (46) found that methylation of PTEN in 49 primary Japanese OSCCs was not common either.…”

Section: Discussionmentioning

confidence: 99%

Methylation of RASSF1A, RASSF2A, and HIN-1 Is Associated with Poor Outcome after Radiotherapy, but not Surgery, in Oral Squamous Cell Carcinoma

Huang

Huang²,

Chen³

et al. 2009

Clinical Cancer Research

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“…The cloning of the PTEN gene was accompanied by detection of various types of mutations including homozygous deletion, frameshift, inframe deletion, truncation, point mutation and so on Shin et al, 2002). Over the last decade following the discovery of this powerful tumor suppressor, numerous PTEN mutations have been identified in a wide range of sporadic malignancies and at a high frequency in cancersusceptibility syndromes.…”

Section: Pten Mutations In Human Cancers: a Database To Be Updatedmentioning

confidence: 99%

PTEN: a new guardian of the genome

2008

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The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) tumor suppressor is a phosphatase that antagonizes the phosphoinositol-3-kinase/AKT signaling pathway and suppresses cell survival as well as cell proliferation. PTEN is the second most frequently mutated gene in human cancer after p53. Germline mutations of PTEN have been found in cancer susceptibility syndromes, such as Cowden syndrome, in which over 80% of patients have mutations of PTEN. Homozygous deletion of Pten causes embryonic lethality, suggesting that PTEN is essential for embryonic development. Mice heterozygous for Pten develop spontaneous tumors in a variety of organs comparable with the spectrum of its mutations in human cancer. The mechanisms of PTEN functions in tumor suppression are currently under intense investigation. Recent studies demonstrate that PTEN plays an essential role in the maintenance of chromosomal stability and that loss of PTEN leads to massive alterations of chromosomes. The tumor suppressor p53 is known as a guardian of the genome that mediates the cellular response to environmental stress, leading to cell cycle arrest or cell death. Through completely different mechanisms, PTEN also protects the genome from instability. Thus, we propose that PTEN is a new guardian of the genome. In this review, we will discuss new discoveries on the role of PTEN in tumor suppression and explore mechanisms by which PTEN maintains genomic stability.

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Inactivation of the PTEN gene by mutation, exonic deletion, and loss of transcript in human oral squamous cell carcinomas

Cited by 22 publications

References 0 publications

PTEN expression and methylation status in oral squamous cell carcinoma

PTEN expression and methylation status in oral squamous cell carcinoma

Methylation of RASSF1A, RASSF2A, and HIN-1 Is Associated with Poor Outcome after Radiotherapy, but not Surgery, in Oral Squamous Cell Carcinoma

PTEN: a new guardian of the genome

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