A novel Ni-based complex inducing apoptosis through mitochondrial dysfunction in osteosarcoma HOS cells
Osteosarcoma, a common primary cancer of the bone in young people, presents major difficulties in medical care because of its resistance to chemotherapy and poor outlook. Consequently, there is an urgent demand for effective and low-toxicity therapeutic approaches. Recently, metal-organic complexes...
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Published in | New journal of chemistry Vol. 48; no. 3; pp. 1362 - 1368 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Cambridge
Royal Society of Chemistry
29.07.2024
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Subjects | |
Online Access | Get full text |
ISSN | 1144-0546 1369-9261 |
DOI | 10.1039/d4nj02041c |
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Abstract | Osteosarcoma, a common primary cancer of the bone in young people, presents major difficulties in medical care because of its resistance to chemotherapy and poor outlook. Consequently, there is an urgent demand for effective and low-toxicity therapeutic approaches. Recently, metal-organic complexes have emerged as promising contenders for anti-cancer investigations. This study includes the successful development of a novel Ni-based complex with 3D supramolecular structure, which was subsequently assessed for its efficacy against osteosarcoma HOS cells. The study also aimed to understand how the complex works on a cellular level. Our experiment results show that the
Ni complex
causes cell cycle arrest in the G0/G1 stage by increasing reactive oxygen species (ROS) levels in HOS cells, disturbing intracellular redox balance, affecting mitochondrial activity, and triggering apoptosis pathways. Furthermore, this study confirms the ability of the
Ni complex
to effectively induce apoptosis in HOS cells. These results not only unveil the potential of the
Ni complex
to trigger apoptosis through ROS-mediated DNA damage mechanisms but also provide a novel therapeutic strategy for osteosarcoma.
A novel
Ni complex
was synthesized and investigated for its impact on the activity of osteosarcoma cells. The results demonstrated a significant elevation in intracellular ROS levels upon exposure to the
Ni complex
in osteosarcoma HOS cells. |
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AbstractList | Osteosarcoma, a common primary cancer of the bone in young people, presents major difficulties in medical care because of its resistance to chemotherapy and poor outlook. Consequently, there is an urgent demand for effective and low-toxicity therapeutic approaches. Recently, metal-organic complexes have emerged as promising contenders for anti-cancer investigations. This study includes the successful development of a novel Ni-based complex with 3D supramolecular structure, which was subsequently assessed for its efficacy against osteosarcoma HOS cells. The study also aimed to understand how the complex works on a cellular level. Our experiment results show that the
Ni complex
causes cell cycle arrest in the G0/G1 stage by increasing reactive oxygen species (ROS) levels in HOS cells, disturbing intracellular redox balance, affecting mitochondrial activity, and triggering apoptosis pathways. Furthermore, this study confirms the ability of the
Ni complex
to effectively induce apoptosis in HOS cells. These results not only unveil the potential of the
Ni complex
to trigger apoptosis through ROS-mediated DNA damage mechanisms but also provide a novel therapeutic strategy for osteosarcoma.
A novel
Ni complex
was synthesized and investigated for its impact on the activity of osteosarcoma cells. The results demonstrated a significant elevation in intracellular ROS levels upon exposure to the
Ni complex
in osteosarcoma HOS cells. Osteosarcoma, a common primary cancer of the bone in young people, presents major difficulties in medical care because of its resistance to chemotherapy and poor outlook. Consequently, there is an urgent demand for effective and low-toxicity therapeutic approaches. Recently, metal–organic complexes have emerged as promising contenders for anti-cancer investigations. This study includes the successful development of a novel Ni-based complex with 3D supramolecular structure, which was subsequently assessed for its efficacy against osteosarcoma HOS cells. The study also aimed to understand how the complex works on a cellular level. Our experiment results show that the Ni complex causes cell cycle arrest in the G0/G1 stage by increasing reactive oxygen species (ROS) levels in HOS cells, disturbing intracellular redox balance, affecting mitochondrial activity, and triggering apoptosis pathways. Furthermore, this study confirms the ability of the Ni complex to effectively induce apoptosis in HOS cells. These results not only unveil the potential of the Ni complex to trigger apoptosis through ROS-mediated DNA damage mechanisms but also provide a novel therapeutic strategy for osteosarcoma. |
Author | Zhang, Zhong Luan, Jian Qin, Yi Li, Li-Long Liu, Xiao-Dong Liu, Pei-Xin |
AuthorAffiliation | Zhuhai Clinical Medical College of Jinan University (Zhuhai People's Hospital) Shenyang University of Chemical Technology College of Science |
AuthorAffiliation_xml | – sequence: 0 name: Shenyang University of Chemical Technology – sequence: 0 name: Zhuhai Clinical Medical College of Jinan University (Zhuhai People's Hospital) – sequence: 0 name: College of Science |
Author_xml | – sequence: 1 givenname: Xiao-Dong surname: Liu fullname: Liu, Xiao-Dong – sequence: 2 givenname: Pei-Xin surname: Liu fullname: Liu, Pei-Xin – sequence: 3 givenname: Zhong surname: Zhang fullname: Zhang, Zhong – sequence: 4 givenname: Li-Long surname: Li fullname: Li, Li-Long – sequence: 5 givenname: Jian surname: Luan fullname: Luan, Jian – sequence: 6 givenname: Yi surname: Qin fullname: Qin, Yi |
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Notes | Electronic supplementary information (ESI) available. CCDC For ESI and crystallographic data in CIF or other electronic format see DOI 2351000 https://doi.org/10.1039/d4nj02041c ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 |
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SubjectTerms | Apoptosis Bone cancer Cell cycle Cellular structure Effectiveness Young adults |
Title | A novel Ni-based complex inducing apoptosis through mitochondrial dysfunction in osteosarcoma HOS cells |
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