Apoptosis induced by retinoic acid in Hep 3B cells in vitro
Human hepatoma Hep 3B cells underwent apoptosis in response to 100 μM all-trans retinoic acid (RA) in full serum (10% fetal calf serum) condition in vitro. Cell death began approximately 24 h following treatment, with more than 80% of the cells dead after 60 h. The dead cells, mainly detached cells,...
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Published in | Cancer letters Vol. 107; no. 1; pp. 149 - 159 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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01.10.1996
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Abstract | Human hepatoma Hep 3B cells underwent apoptosis in response to 100 μM all-trans retinoic acid (RA) in full serum (10% fetal calf serum) condition in vitro. Cell death began approximately 24 h following treatment, with more than 80% of the cells dead after 60 h. The dead cells, mainly detached cells, exhibited condensed chromatin and DNA fragmentation, which are indicative of endonuclease activation and are the hallmarks of apoptosis in epithelial cells. Concurrent exposure to 1 μM cycloheximide (CX) prevented approximately 50% of cell death and DNA fragmentation induced by RA. Thus, other toxic injury to the cells as well as apoptosis might be involved in cell death. Sixty hours exposure of RA decreased the percentage of cells in G
1 phase (16.3 ± 0.4% versus 52.4 ± 2.1%;
P ≤ 0.01) and in G
2/M phase (13.4 ± 1.2% versus 21.2 ± 0.7%;
P ≤ 0.01), but did not change percent of cells in S phase (20.8 ± 0.2% versus 20.7 ± 0.5%) of the cell cycle compared with control. RA may have caused accumulation of Hep 3B cells before G
1 phase, and that
G
0
G
1
transition is a main check point in the active process of apoptosis. Electron micrographs of the cells treated with RA revealed typical morphologic changes of apoptosis, besides toxic injury to the cells. These data strongly indicate that RA is able to induce apoptosis and the induction of apoptosis may contribute to the antitumor activity of RA against hepatoma cells. |
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AbstractList | Human hepatoma Hep 3B cells underwent apoptosis in response to 100 μM all-trans retinoic acid (RA) in full serum (10% fetal calf serum) condition in vitro. Cell death began approximately 24 h following treatment, with more than 80% of the cells dead after 60 h. The dead cells, mainly detached cells, exhibited condensed chromatin and DNA fragmentation, which are indicative of endonuclease activation and are the hallmarks of apoptosis in epithelial cells. Concurrent exposure to 1 μM cycloheximide (CX) prevented approximately 50% of cell death and DNA fragmentation induced by RA. Thus, other toxic injury to the cells as well as apoptosis might be involved in cell death. Sixty hours exposure of RA decreased the percentage of cells in G
1 phase (16.3 ± 0.4% versus 52.4 ± 2.1%;
P ≤ 0.01) and in G
2/M phase (13.4 ± 1.2% versus 21.2 ± 0.7%;
P ≤ 0.01), but did not change percent of cells in S phase (20.8 ± 0.2% versus 20.7 ± 0.5%) of the cell cycle compared with control. RA may have caused accumulation of Hep 3B cells before G
1 phase, and that
G
0
G
1
transition is a main check point in the active process of apoptosis. Electron micrographs of the cells treated with RA revealed typical morphologic changes of apoptosis, besides toxic injury to the cells. These data strongly indicate that RA is able to induce apoptosis and the induction of apoptosis may contribute to the antitumor activity of RA against hepatoma cells. Human hepatoma Hep 3B cells underwent apoptosis in response to 100 microM all-trans retinoic acid (RA) in full serum (10% fetal calf serum) condition in vitro. Cell death began approximately 24 h following treatment, with more than 80% of the cells dead after 60 h. The dead cells, mainly detached cells, exhibited condensed chromatin and DNA fragmentation, which are indicative of endonuclease activation and are the hallmarks of apoptosis in epithelial cells. Concurrent exposure to 1 microM cycloheximide (CX) prevented approximately 50% of cell death and DNA fragmentation induced by RA. Thus, other toxic injury to the cells as well as apoptosis might be involved in cell death. Sixty hours exposure of RA decreased the percentage of cells in G1 phase (16.3 +/- 0.4% versus 52.4 +/- 2.1%; P < or = 0.01) and in G2/M phase (13.4 +/- 1.2% versus 21.2 +/- 0.7%; P < or = 0.01), but did not change percent of cells in S phase (20.8 +/- 0.2% versus 20.7 +/- 0.5%) of the cell cycle compared with control. RA may have caused accumulation of Hep 3B cells before G1 phase, and that G0/G1 transition is a main check point in the active process of apoptosis. Electron micrographs of the cells treated with RA revealed typical morphologic changes of apoptosis, besides toxic injury to the cells. These data strongly indicate that RA is able to induce apoptosis and the induction of apoptosis may contribute to the antitumor activity of RA against hepatoma cells. |
Author | You, Kyung Ran Ahn, Deuk Soo Kim, Dae Ghon Jo, Baik Hwan |
Author_xml | – sequence: 1 givenname: Dae Ghon surname: Kim fullname: Kim, Dae Ghon organization: Division of GI and Hepatology, Department of Internal Medicine, Chonbuk National University Medical School, Keumamdong 634-18, Dukjinku, Chonju, Chonbuk, 560-182, South Korea – sequence: 2 givenname: Baik Hwan surname: Jo fullname: Jo, Baik Hwan organization: Department of General Surgery, Institute for Medical Science, Chunbuk National University Medical School, Chonju, Chonhuk 560-182, South Korea – sequence: 3 givenname: Kyung Ran surname: You fullname: You, Kyung Ran organization: Division of GI and Hepatology, Department of Internal Medicine, Chonbuk National University Medical School, Keumamdong 634-18, Dukjinku, Chonju, Chonbuk, 560-182, South Korea – sequence: 4 givenname: Deuk Soo surname: Ahn fullname: Ahn, Deuk Soo organization: Division of GI and Hepatology, Department of Internal Medicine, Chonbuk National University Medical School, Keumamdong 634-18, Dukjinku, Chonju, Chonbuk, 560-182, South Korea |
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Keywords | Hep 3B cells Retinoic acid Hepatom Apoptosis Antineoplastic agent Human Hepatic disease Malignant tumor Retinoids In vitro Liver cell carcinoma Cell death Established cell line Digestive diseases Tumor cell |
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Snippet | Human hepatoma Hep 3B cells underwent apoptosis in response to 100 μM all-trans retinoic acid (RA) in full serum (10% fetal calf serum) condition in vitro.... Human hepatoma Hep 3B cells underwent apoptosis in response to 100 microM all-trans retinoic acid (RA) in full serum (10% fetal calf serum) condition in vitro.... |
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SubjectTerms | Antineoplastic agents Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Apoptosis - genetics Biological and medical sciences Carcinoma, Hepatocellular - pathology Cell Cycle - drug effects Cycloheximide - pharmacology DNA, Neoplasm - analysis General aspects Hep 3B cells Hepatom Humans Liver Neoplasms - pathology Medical sciences Microscopy, Electron Pharmacology. Drug treatments Protein Synthesis Inhibitors - pharmacology Retinoic acid Tretinoin - pharmacology |
Title | Apoptosis induced by retinoic acid in Hep 3B cells in vitro |
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