Saini Nitin, Srinivasan Radhika, Chawla Yogesh, Sharma Sanjeev, Chakraborti Anuradha, Rajwanshi Arvind
Department of Hepatology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Liver Int. 2009 Sep;29(8):1162-70. doi: 10.1111/j.1478-3231.2009.02082.x. Epub 2009 Jul 17.
Telomerase expression and the maintenance of a critical telomere length (TL) in cancer initiation indicates that telomere shortening and telomerase expression initiates cancer by induction of chromosomal instability.
Telomerase activity, TL and human telomerase reverse transcriptase (hTERT) expression were investigated in 58 hepatocellular carcinoma (HCC) and 17 chronic hepatitis patients by the telomerase repeat amplification protocol, Southern blotting and reverse transcriptase-polymerase chain reaction.
Telomerase was positive in 76% of HCC and 11.8% of chronic hepatitis patients (P<0.0001). The mean telomere length (MTL) in HCC was significantly shorter compared with chronic hepatitis (P<0.0001). The MTL was not significantly different in HCC patients with and without cirrhosis (P=0.77). In hepatitis B virus, hepatitis C virus and non-B non-C-related HCC groups, no differences were found in telomerase activity and MTL (P=0.77). hTERT, a regulator of telomerase, was, however, positive in 81% of HCCs. The correlation between telomerase activity and hTERT mRNA expression was statistically significant (P<0.0001). The MTL in telomerase-positive HCC cases was significantly shorter than the MTL in telomerase-negative cases (P<0.0001).
The majority of HCCs exhibited telomerase activity that correlated well with hTERT expression. MTL in HCC was significantly shorter than chronic hepatitis. It was also found that shorter telomeres are present in telomerase-positive HCC cases. However, no correlation was found between telomerase activity and TL with respect to the viral status in HCC.
端粒酶表达以及癌症起始过程中关键端粒长度（TL）的维持表明，端粒缩短和端粒酶表达通过诱导染色体不稳定引发癌症。
采用端粒酶重复序列扩增法、Southern印迹法和逆转录聚合酶链反应，对58例肝细胞癌（HCC）患者和17例慢性肝炎患者的端粒酶活性、TL及人端粒酶逆转录酶（hTERT）表达进行研究。
76%的HCC患者端粒酶呈阳性，慢性肝炎患者中这一比例为11.8%（P<0.0001）。与慢性肝炎相比，HCC患者的平均端粒长度（MTL）显著缩短（P<0.0001）。有肝硬化和无肝硬化的HCC患者MTL无显著差异（P=0.77）。在乙型肝炎病毒、丙型肝炎病毒及非乙非丙相关HCC组中，端粒酶活性和MTL无差异（P=0.77）。然而，端粒酶的调节因子hTERT在81%的HCC中呈阳性。端粒酶活性与hTERT mRNA表达之间的相关性具有统计学意义（P<0.0001）。端粒酶阳性HCC病例的MTL显著短于端粒酶阴性病例（P<0.0001）。
大多数HCC表现出端粒酶活性，且与hTERT表达密切相关。HCC的MTL显著短于慢性肝炎。还发现端粒酶阳性HCC病例中端粒较短。然而，就HCC的病毒状态而言，端粒酶活性与TL之间未发现相关性。
