Expression of PTEN and Its Correlation with Proliferation Marker Ki-67 in Head and Neck Cancer. Issue 2 (April 2016)

• Record Type: Journal Article
• Authors: Ahmed, Malik W.; Kayani, Mahmood A.; Shabbir, Ghulam; Ali, Syed M.; Shinwari, Wajih-ud-Din; Mahjabeen, Ishrat
• Is Part Of: International journal of biological markers. Volume 31:Issue 2(2016)
• Page Start: 193
• Page End: 203
• Publication Date: 2016-04
• Subjects: Expression analysis -- Ki-67 -- HNC -- PTEN -- qPCR; Cell receptors -- Periodicals; Histochemistry -- Periodicals; Tumor markers -- Periodicals; Tumor antigens -- Periodicals; 616.99407582
• DOI: 10.5301/jbm.5000196
• Languages: English
• ISSNs: 0393-6155

Abstract

Introduction: PTEN is part of large family of tyrosine phosphatases and has been found inactivated in a wide variety of human cancers. Aims: In the present study we have tried to determine the association of the expression patterns of this gene with carcinogenesis. Methods: First, a systematic review was carried out to ascertain the importance of the PTEN gene and its role in carcinogenesis. In the second phase, a case-control study was designed using different expression analysis techniques. Expression of PTEN mRNA was analyzed using reverse transcriptase polymerase chain reaction (RT-PCR). Results: Significantly downregulated expression of PTEN was observed in patients with head and neck cancer (HNC) compared to adjacent normal-tissue controls. These results were confirmed with quantitative polymerase chain reaction (qPCR). Significant downregulation of the gene was observed in HNC patients compared to adjacent normal-tissue controls. PTEN expression was correlated with different histopathological parameters of the study cohort by Spearman's correlation coefficient and a significant negative correlation was observed with pT stage (r = −0.271*; p<0.02) and grade (r = −0.228*; p<0.02) of HNC tissues. Furthermore, the expression variations of PTEN were correlated with the expression pattern of the proliferation marker Ki-67. Significantly (p<0.008) upregulated expression of Ki-67 was observed in HNC patients compared with adjacent normal-tissue controls This upregulation of Ki-67 was confirmed at the protein level by immunohistochemistry in HNC patients. When Spearman's correlation was carried out a significant negative correlation was observed between PTEN and Ki-67 (r = −0.230*; p<0.03). Conclusions: Our data suggest that downregulation of PTEN and overexpression of Ki-67 may contribute to the initiation and progression of HNC.