Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells
Abstract Objective Primary tumors of the brain and a large percent of malignant brain tumors are gliomas. Gliomas comprise high-grade gliomas like glioblastoma multiforme (GBMs), many of which have mutation in the tumor suppressor p53 gene and low-grade gliomas (LGGs). LGGs can progress to GBMs due...
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2025-01-01
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| Online Access: | https://doi.org/10.1186/s13104-025-07092-8 |
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| author | Yoo Na Kim Ketki Patil S. Balakrishna Pai |
| author_facet | Yoo Na Kim Ketki Patil S. Balakrishna Pai |
| author_sort | Yoo Na Kim |
| collection | DOAJ |
| description | Abstract Objective Primary tumors of the brain and a large percent of malignant brain tumors are gliomas. Gliomas comprise high-grade gliomas like glioblastoma multiforme (GBMs), many of which have mutation in the tumor suppressor p53 gene and low-grade gliomas (LGGs). LGGs can progress to GBMs due to various factors. The available treatment options for GBMs and LGGs include surgical resection, radiation and chemotherapy. The chemotherapeutic drug available in the clinic is temozolomide (TMZ). However, TMZ can cause damage to DNA if taken for prolonged period. This warrants the discovery of drugs that would potentially elicit less adverse side effects while maintaining anticancer activity. To this end, we evaluated the impact of cinnamaldehyde (CA), a single, purified component of the natural product cinnamon. Results The elucidation of the mechanism of action revealed the impact of CA on reactive oxygen species (ROS) levels. Moreover, its effect on the extrinsic programmed cell death pathway resulted in the increase of apoptotic cell populations, invoking multicaspase. Notably, the cell survival/death pivotal molecule Bcl-2 was impacted. These effects were observed in both the types of brain tumor cells studied: GBMs, represented by U251 cells (p53 mutated cell line) and LGGs represented by H4 cells. Results from the current study suggest potential for CA as a therapeutic option as it is expected to have fewer adverse side effects due to it being a component of a natural product and possibly deter the progression of LGGs to GBMs. |
| format | Article |
| id | doaj-art-82706b4cda4e49c88cbbf99c40b6f816 |
| institution | Kabale University |
| issn | 1756-0500 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Research Notes |
| spelling | doaj-art-82706b4cda4e49c88cbbf99c40b6f8162025-01-26T12:13:19ZengBMCBMC Research Notes1756-05002025-01-011811710.1186/s13104-025-07092-8Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cellsYoo Na Kim0Ketki Patil1S. Balakrishna Pai2Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory UniversityWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory UniversityWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory UniversityAbstract Objective Primary tumors of the brain and a large percent of malignant brain tumors are gliomas. Gliomas comprise high-grade gliomas like glioblastoma multiforme (GBMs), many of which have mutation in the tumor suppressor p53 gene and low-grade gliomas (LGGs). LGGs can progress to GBMs due to various factors. The available treatment options for GBMs and LGGs include surgical resection, radiation and chemotherapy. The chemotherapeutic drug available in the clinic is temozolomide (TMZ). However, TMZ can cause damage to DNA if taken for prolonged period. This warrants the discovery of drugs that would potentially elicit less adverse side effects while maintaining anticancer activity. To this end, we evaluated the impact of cinnamaldehyde (CA), a single, purified component of the natural product cinnamon. Results The elucidation of the mechanism of action revealed the impact of CA on reactive oxygen species (ROS) levels. Moreover, its effect on the extrinsic programmed cell death pathway resulted in the increase of apoptotic cell populations, invoking multicaspase. Notably, the cell survival/death pivotal molecule Bcl-2 was impacted. These effects were observed in both the types of brain tumor cells studied: GBMs, represented by U251 cells (p53 mutated cell line) and LGGs represented by H4 cells. Results from the current study suggest potential for CA as a therapeutic option as it is expected to have fewer adverse side effects due to it being a component of a natural product and possibly deter the progression of LGGs to GBMs.https://doi.org/10.1186/s13104-025-07092-8High-grade gliomaLow-grade gliomaCinnamaldehydeU251H4Apoptosis |
| spellingShingle | Yoo Na Kim Ketki Patil S. Balakrishna Pai Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells BMC Research Notes High-grade glioma Low-grade glioma Cinnamaldehyde U251 H4 Apoptosis |
| title | Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells |
| title_full | Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells |
| title_fullStr | Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells |
| title_full_unstemmed | Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells |
| title_short | Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells |
| title_sort | cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high grade and low grade human glioma cells |
| topic | High-grade glioma Low-grade glioma Cinnamaldehyde U251 H4 Apoptosis |
| url | https://doi.org/10.1186/s13104-025-07092-8 |
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