The imprinting status of genetic imprinted gene PEG10 in human hepatocellular carcinomas / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the imprinting status of genetic imprinted gene PEG10 (perternally expressed gene 10) in human hepatocellular carcinoma (HCC) tissues and liver cancer cell lines.</p><p><b>METHODS</b>Genomic DNA was extracted from 20 HCC tissues and its adjacent tissues, 15 normal liver tissues, 5 liver cancer cell lines (PLC/PRF/5, smmc-7721, HepG2, Hep3B, SK-HEP-1) and 2 normal human liver cell lines (changliver, HL7702). The DNA fragments containing single nucleotide polymorphism (SNP) site of PEG10 were amplified by polymerase chain reaction (PCR) and the genotype of samples was detected by DNA sequencing. Total RNA was extracted from heterozygous samples, the imprinting status and expression level of PEG10 were evaluated by quantitative real time reverse transcription-polymerase chain reaction (qRT-PCR) and DNA sequencing.</p><p><b>RESULTS</b>It was found that 16/40 of HCC and its adjacent tissues were heterozygous, 3/15 of normal liver tissue were heterozygous. A site of heterozygous mutation was found in HepG2 cells by DNA sequencing. The other liver tissues and cell lines were all homozygous. PEG10 was biallelically expressed and showed loss of imprinting (LOI) in 82.4% (14/17) liver cancer samples (16 HCC tissues and HepG2), however it was a monoallelic expression and showed genomic imprinting in17.6% (3/17) liver cancer samples. In HCC, the expression levels of PEG10 were increased apparently, but it was negative expressed in cancer adjacent tissues and normal liver tissues. Expression levels of PEG10 were not significantly different between imprinted HCC tissues and HCC tissues with LOI (t = 1.311, P value is more than 0.05).</p><p><b>CONCLUSION</b>PEG10 imprinting is lost in a majority of HCC and no correlation exists between the imprinting status of PEG10 and its expressions in HCC tissues.</p>

An oncosis-like cell death of pancreatic cancer Panc-1 cells induced by artesunate is related to generation of reactive oxygen species / 中国癌症杂志

50?mol/L induced markedly oncotic cell death,but no apoptosis was observed.TEM examination indicated that a form of cell death accompanied by cellular swelling,organelle swelling and vacuolization,mitochondrial swelling and cristae membrane loss,and nucleus swelling, chromatin scattering or karyolysis,which characterized as oncosis.When treated with 50,200?mol/L of ART for 5 h, the intracellular ROS level of Panc-1 cells markedly increased to 1.60 and 4.49 fold compared with that of untreated cells,respectively.Pretreatment with TCEP effectively attenuated ART-induced intracellular ROS level and decrease the oncosis in Panc-1 cells.Conclusions:ART exerts profound cytotoxic effects on Panc-1 cells and induces an oncosis- like cell death,which is quite different from apoptosis.The cellular generation of ROS and its peroxidation damage may be one of the mechanisms for its anti-tumor effect on pancreatic cancer.