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Published on: October 30, 2013
The apoptotic process of human bladder carcinoma T24 cells induced by retinoid
Chung-Liang Chien1, Tung-Wei Chen, Yi-Shan Lin
1Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan. clc@ha.mc.ntu.edu.tw
Abstract:
Breakdown of the cytoskeletal network and redistribution of cytoplasmic organelles are early events of programmed cell death. Previous studies showed that retinoic acid induces programmed cell death in many tumor cell lines and that cytokeratins, particularly cytokeratin 18, are affected in the early events of apoptosis. In this study, patterns of cytoplasmic intermediate filaments (cytokeratin 18), actin filaments, and microtubules, as well as Bax and Bcl-2 proteins in human bladder carcinoma T24 cells were examined before and after retinoic acid treatment by immunocytochemistry and conventional electron microscopy. Our results demonstrate that the redistribution of Bax and Bcl-2 proteins in the subcellular compartment of T24 cells is correlated with reorganization of the cytoplasmic intermediate filament network and that cytokeratins are cleaved by caspases, as revealed by the M30 antibody which recognizes a specific caspase cleavage site within cytokeratin 18. The cytoskeletal architectures of microtubules are not significantly affected in the early apoptotic process, from our observations. We suggest that the breakdown in the intermediate filament network associated with the aggregation of mitochondria and lysosome may be a crucial event in the apoptotic process and that aggregation of cytoplasmic Bax may accelerate apoptotic death.
Insights
Retinoic acid triggers programmed cell death by altering intermediate filaments and protein distribution in bladder cancer cells. This cytoskeletal reorganization, involving cytokeratin 18 cleavage, is a key event in apoptosis.
Area of Science:
- Cell Biology
- Cancer Research
- Biochemistry
Background:
- Programmed cell death (apoptosis) involves cytoskeletal breakdown and organelle redistribution.
- Retinoic acid is known to induce apoptosis in various tumor cell lines.
- Cytokeratins, especially cytokeratin 18, are implicated in early apoptotic events.
Purpose of the Study:
- To investigate the effects of retinoic acid on cytoskeletal elements (intermediate filaments, actin, microtubules) and apoptosis-related proteins (Bax, Bcl-2) in human bladder carcinoma T24 cells.
- To correlate changes in protein localization with cytoskeletal reorganization during retinoic acid-induced apoptosis.
- To identify specific molecular events, such as caspase cleavage of cytokeratins, during early apoptosis.
Main Methods:
- Immunocytochemistry was used to visualize intermediate filaments (cytokeratin 18), actin filaments, microtubules, Bax, and Bcl-2 proteins.
- Conventional electron microscopy provided ultrastructural details of cellular changes.
- The M30 antibody was employed to detect caspase-mediated cleavage of cytokeratin 18.
Main Results:
- Retinoic acid treatment induced redistribution of Bax and Bcl-2 proteins, correlating with intermediate filament network reorganization.
- Caspase-dependent cleavage of cytokeratins (cytokeratin 18) was confirmed by M30 antibody staining.
- Microtubule architecture remained largely unaffected in the early stages of apoptosis.
- Aggregation of mitochondria and lysosomes was observed alongside intermediate filament breakdown.
Conclusions:
- The breakdown of the intermediate filament network and aggregation of organelles are critical early events in retinoic acid-induced apoptosis.
- Subcellular redistribution of Bax and Bcl-2 proteins is linked to cytoskeletal reorganization.
- Cleavage of cytokeratin 18 by caspases is a significant molecular marker of early apoptosis.
- Aggregation of cytoplasmic Bax may accelerate the apoptotic process in T24 cells.
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