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1.
Journal of International Oncology ; (12): 700-704, 2022.
Article in Chinese | WPRIM | ID: wpr-954348

ABSTRACT

Endometrial cancer has been identified by The Cancer Genome Atlas program with four molecular subtypes by genome sequence analysis. Clinical trials to select suitable immunotherapeutic agents based on the different immune characteristics of each subtype have been conducted in several countries and have made important progress. The main clinical applications of immune checkpoint inhibitors include anti-programmed cell death protein-1/programmed death-ligand 1 antibodies and poly ADP-ribose polymerase inhibitors. Optimizing drug selection and drug combination based on the target characteristics of different immune checkpoint inhibitors may provide new opportunities for immunotherapy of endometrial cancer and bring new light to improve survival rates.

2.
Chinese Medical Sciences Journal ; (4): 44-50, 2004.
Article in English | WPRIM | ID: wpr-254030

ABSTRACT

<p><b>OBJECTIVE</b>To search novel method for diagnosis and therapy of B-lymphoma, specific small molecular peptide ligands against binding site of tumor cells were screened and its effects on signal transduction and cell apoptosis were tested.</p><p><b>METHODS</b>Specific peptide ligands were screened by binding with site of human B lymphoma cell (OC1LY8) using peptide-bead libraries. The identified peptides were characterized with responsible cells by rebinding test. The role of tyrosine phosphorylation of peptide ligand was tested by Western blot; and its apoptosispromoting role was observed by confocal fluorescent microscope.</p><p><b>RESULTS</b>Specific peptide ligand was able to bind specifically to site on cell surface and enter into cytoplasm. Tetrameric peptide ligand was able to strongly trigger signal transduction resulting in tyrosine phosphorylation and cellular apoptosis in OC1LY8 cell line.</p><p><b>CONCLUSION</b>Screened peptide ligand can effectively bind with OC1LY8 cell, stimulate cellular tyrosine phosphorylation and induce cellular apoptosis.</p>


Subject(s)
Humans , Amino Acid Sequence , Apoptosis , Cell Line, Tumor , Ligands , Lymphoma, B-Cell , Metabolism , Pathology , Oligopeptides , Chemistry , Pharmacology , Peptide Library , Phosphorylation , Signal Transduction , Tyrosine , Metabolism
3.
Chinese Medical Journal ; (24): 742-746, 2003.
Article in English | WPRIM | ID: wpr-324420

ABSTRACT

<p><b>OBJECTIVE</b>To assess the effects of nuclear translocation of tissue transglutaminase (TTG) and the release of cytochrome C on hepatocyte apoptosis and to reveal the mechanism of signal transduction of early apoptosis in injured hepatocytes.</p><p><b>METHODS</b>Hepatocytes isolated from tissue transglutaminase gene knock-out mice and rats were stimulated with ethanol. Proteins from whole cell, cytoplasm and nuclei were extracted for determination of TTG activity by (14)C-putrescine incorporation. Distribution of TTG throughout the entire cell, as well as just nucleus was observed under a confocal scanning microscope. The amount of cytochrome C released from mitochondria was determined by ELISA. Cell apoptosis was observed by fluorescent cytochemistry.</p><p><b>RESULTS</b>TTG activity in whole cells and nuclei was significantly increased after the hepatocytes were treated with ethanol. Cytochrome C release was remarkably increased in the cells isolated from rat and wild-type mouse after treatment with ethanol but not in TTG gene knock-out mice. Cellular apoptosis appeared in hepatocytes isolated from rats and wild-type mice but not in the hepatocytes from TTG gene knock-out mice after stimulation with ethanol.</p><p><b>CONCLUSIONS</b>Increased TTG in hepatocytes can be translocated into the nucleus and promote release of mitochondrial cytochrome C into the cytoplasm. Passing through a series of signal pathways, hepatocyte apoptosis is induced eventually.</p>


Subject(s)
Animals , Male , Mice , Rats , Apoptosis , Cell Nucleus , Metabolism , Cytochrome c Group , Metabolism , Hepatocytes , Cell Biology , Metabolism , Signal Transduction , Transglutaminases , Metabolism
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