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Thymosin β₄ knockdown disrupts mitochondrial functions of SW480 human colon cancer cells
1Institute of Biopharmaceutical Sciences, School of Life Sciences, National Yang-Ming University, Taipei, Taiwan.
Abstract:
Thymosin β(4) (Tβ(4)), overexpressed in various tumors, has been shown to be involved in cellular anti-oxidation. Reactive oxygen species (ROS) function as signaling molecules and play certain roles in tumor progression. To assess the anti-oxidative role of endogenous Tβ(4) in tumor cells, its expression in SW480 cells was knocked down by a shRNA, which induced significant increases of ROS. Interestingly, some cristae-lost and several electron-dense mitochondria appeared in cells with Tβ(4) knockdown that was accompanied by a marked decline of the membrane potential of these organelles. Strikingly, while the ATP and lactate levels in SW480 cells were notably elevated by Tβ(4) downregulation, this treatment significantly diminished the mitochondrial DNA copy number and protein levels of several subunits of the electron transport complexes. Finally, immunofluorescent staining results suggested the presence of Tβ(4) in mitochondria. To the best of our knowledge, this is the first report to demonstrate that Tβ(4) knockdown can disrupt the morphology and some crucial functions of mitochondria in human colorectal carcinoma (CRC) cells.
Insights
Thymosin beta-4 (Tβ(4)) knockdown in colorectal cancer cells increased reactive oxygen species and disrupted mitochondria. This study reveals Tβ(4)
Area of Science:
- Cell Biology
- Biochemistry
- Oncology
Background:
- Thymosin beta-4 (Tβ(4)) is overexpressed in tumors and linked to cellular anti-oxidation.
- Reactive oxygen species (ROS) are signaling molecules involved in tumor progression.
Purpose of the Study:
- To investigate the anti-oxidative role of endogenous Tβ(4) in tumor cells.
- To determine the impact of Tβ(4) knockdown on mitochondrial function and morphology in colorectal carcinoma (CRC) cells.
Main Methods:
- Tβ(4) expression was reduced in SW480 cells using shRNA.
- ROS levels, mitochondrial morphology, membrane potential, ATP and lactate levels, and mitochondrial DNA copy number were assessed.
- Protein levels of electron transport chain complexes and Tβ(4) localization were analyzed.
Main Results:
- Tβ(4) knockdown led to increased ROS levels and altered mitochondrial morphology (cristae loss, electron-dense mitochondria).
- Mitochondrial membrane potential declined, while ATP and lactate levels increased.
- Mitochondrial DNA copy number and electron transport complex subunit levels were diminished.
- Immunofluorescence confirmed Tβ(4) presence in mitochondria.
Conclusions:
- Tβ(4) plays a crucial role in maintaining mitochondrial integrity and function in human CRC cells.
- Tβ(4) knockdown disrupts mitochondrial morphology and key functions, impacting cellular metabolism.
- This is the first report demonstrating Tβ(4)'s role in mitochondrial regulation within CRC.
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