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1. Exposure of Human Lung Cancer Cells to 8-Chloro-Adenosine Induces G2/M Arrest and Mitotic Catastrophe

Author

Hong-Yu Zhang, Yan-Yan Gu, Zeng-Gang Li, Yu-Hong Jia, Lan Yuan, Shu-Yan Li, Guo-Shun An, Ju-Hua Ni, and Hong-Ti Jia

Subjects
8-chloro-adenosine, cytotoxicity, G2/M arrest, mitotic catastrophe, apoptosis, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

8-Chloro-adenosine (8-CI-Ado) is a potent chemotherapeutic agent whose cytotoxicity in a variety of tumor cell lines has been widely investigated. However, the molecular mechanisms are uncertain. In this study, we found that exposure of human lung cancer cell lines A549 (p53-wt) and H1299 (p53-depleted) to 8-CI-Ado induced cell arrest in the G2/M phase, which was accompanied by accumulation of binucleated and polymorphonucleated cells resulting from aberrant mitosis and failed cytokinesis. Western blotting showed the loss of phosphorylated forms of Cdc2 and Cdc25C that allowed progression into mitosis. Furthermore, the increase in Ser10-phosphorylated histone H3-positive cells revealed by fluorescence-activated cell sorting suggested that the agent-targeted cells were able to exit the G2 phase and enter the M phase. Immunocytochemistry showed that microtubule and microfilament arrays were changed in exposed cells, indicating that the dynamic instability of microtubules and microfilaments was lost, which may correlate with mitotic dividing failure. Aberrant mitosis resulted in mitotic catastrophe followed by varying degrees of apoptosis, depending on the cell lines. Thus, 8-CI-Ado appears to exert its cytotoxicity toward cells in culture by inducing mitotic catastrophe.

Published
2004
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2. [Deletion of p15 and p16 genes and overexpression of STK15 gene in human laryngeal squamous cell carcinoma]

Author

Fu-cai, Li, Ying-hui, Li, Xu, Zhao, Ning, Kang, Wei-neng, Fu, Zhen-ming, Xu, Zeng-gang, Li, and Kai-lai, Sun

Subjects
Aurora Kinases, Reverse Transcriptase Polymerase Chain Reaction, Genes, p16, Tumor Suppressor Proteins, Carcinoma, Squamous Cell, Humans, Cell Cycle Proteins, Protein Serine-Threonine Kinases, Laryngeal Neoplasms, Gene Deletion, Aurora Kinase A, Cyclin-Dependent Kinase Inhibitor p15
Abstract

To investigate the association of p15 and p16 genes deletion, and STK15 gene overexpression with laryngeal squamous cell carcinoma (LSCC).The cancer tissue and surrounding normal tissue were taken during operation from 50 cases of LSCC who had undergone neither chemotherapy nor radiotherapy preoperatively. DNA was extracted and PCR was used to test the homozygous deletion of p15 exon 2 (p15E2) and p16 exon 2 (p16E2). RNA was extracted, cDNA was synthesized by reverse transcription, and the expression of STK15 gene was tested by PCR with beta-actin as inner control. At the same time the expression of STK15 in human LSCC Hep-2 cell line was tested. The ratio of ADV (average density value) of STK15 gene to the ADV of beta-actin gene was calculated.The rate of p15E2 deletion was 12% (6/50) and that of p16E2 was 14% (7/50). The p15E2 and p16E2 codeletion rate was 6% (3/50). In 34 of the 50 cases (68%) the expression of STK15 gene in tumor tissue was higher than that of the paired surrounding normal tissue with a significant difference. The ratio of ADV of STK15 gene to ADV of beta-actin gene was 1.03 +/- 0.30 in the cancer tissue, and 0.89 +/- 0.22 in the paired normal tissue with a significant difference (t = 4.333, P0.01). The expression of STK15 gene was higher than that of beta-actin in Hep-2 cell line.The homozygous deletion of p15E2 and p16E2 and overexpression of STK15 gene may play a role in the oncogenesis and malignant progression of laryngeal squamous cell carcinoma.

Published
2003

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