This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
xiaoguang chen
Henan University of Science and Technology
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Dodecanoic acid (DDA), a medium chain saturated fatty acids, has been reported to have anticancer activity in reproductive system cancer and some digestive tract cancers. However, the role and the underlying mechanism of DDA in liver cancer have been rarely defined.
Methods
Mouse liver cancer Hepa 1–6 cells were administrated with DDA in this present study. Apoptosis, cell cycle analysis, mitochondrial membrane potential (MMP) and ATP content were determined by flow cytometry; GSH availability, ROS level and SOD activity was assessed by a microplate reader; Bcl-2, Bax and Caspase-3 protein levels were analyzed by western blot.
Results
0.5 mM DDA was identified as the ideal concentration for investigation and could time-dependently inhibit cell viability. DDA-treated cells had a significant, time-dependent increase in cell apoptotic rate in spite of an accumulation of the cells in S + G2/M phase of the cell cycle. The enhanced level of ROS, depletion of GSH and the reduced activity of SOD in DDA-treated cells indicated the generation of oxidative stress; mitochondrial dysfunction was evidenced by the dissipation of MMP of and the reduction in ATP content. Cell death via mitochondrial pathway was indicated by the reduced Bcl-2/Bax ratio and the increased level of caspase-3 protein.
Conclusions
Taken together, DDA effectively triggers oxidative stress-induced death in liver cancer cells by disturbing the structure and function of mitochondria. The findings provide an in-depth insight into the potential action mechanism of DDA on liver cancer.
Keywords
Medium chain fatty acid, Dodecanoic acid, Liver cancer, Oxidative damage, Apoptosis, Mitochondria
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
xiaoguang chen
Henan University of Science and Technology
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 01 Dec, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Dodecanoic acid (DDA), a medium chain saturated fatty acids, has been reported to have anticancer activity in reproductive system cancer and some digestive tract cancers. However, the role and the underlying mechanism of DDA in liver cancer have been rarely defined.
Methods
Mouse liver cancer Hepa 1–6 cells were administrated with DDA in this present study. Apoptosis, cell cycle analysis, mitochondrial membrane potential (MMP) and ATP content were determined by flow cytometry; GSH availability, ROS level and SOD activity was assessed by a microplate reader; Bcl-2, Bax and Caspase-3 protein levels were analyzed by western blot.
Results
0.5 mM DDA was identified as the ideal concentration for investigation and could time-dependently inhibit cell viability. DDA-treated cells had a significant, time-dependent increase in cell apoptotic rate in spite of an accumulation of the cells in S + G2/M phase of the cell cycle. The enhanced level of ROS, depletion of GSH and the reduced activity of SOD in DDA-treated cells indicated the generation of oxidative stress; mitochondrial dysfunction was evidenced by the dissipation of MMP of and the reduction in ATP content. Cell death via mitochondrial pathway was indicated by the reduced Bcl-2/Bax ratio and the increased level of caspase-3 protein.
Conclusions
Taken together, DDA effectively triggers oxidative stress-induced death in liver cancer cells by disturbing the structure and function of mitochondria. The findings provide an in-depth insight into the potential action mechanism of DDA on liver cancer.
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