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Research Article
Wei-Jing Gong
Wuhan Union Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-2114-7514
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Lung cancer is the most commonly diagnosed cancer with a high mortality rate. Cisplatin is one of the most important chemotherapeutic agents for the treatment of lung cancer patients, especially in advanced stages. Recent studies showed that cisplatin may interact with mitochondria which may partly account for its cytotoxicity. In the study, we explored the effect of resistin on cisplatin-induced cytotoxicity in A549 cells and assessed whether mitochondria-dependent apoptosis was involved. Our results found that 25 ng/ml resistin could significantly increase cisplatin-induced apoptosis and G2/M phase arrest, enhance reactive oxygen species generation, exacerbate the collapse of mitochondrial membrane potential, promote the distribution of cytochrome C in the cytoplasm from mitochondria, and activate caspase 3. Therefore, the results suggested that resistin might increase cisplatin-induced cytotoxicity via a mitochondria-mediated pathway in A549 cells. However, the precise mechanism has yet to be explored in the future.
Keywords
cisplatin, lung cancer, resistin, mitochondria
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CURRENT STATUS: Under Revision
Version 1
Posted 10 Mar, 2021
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Editorial decision: Major Revisions Needed
On 29 Mar, 2021
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Received 06 Mar, 2021
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Invitations sent on 05 Mar, 2021
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On 22 Feb, 2021
First submitted
On 21 Feb, 2021
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Subject Areas
Oncology
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This preprint is under consideration at Medical Oncology. A preprint is 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.
Learn more about In Review
Research Article
Wei-Jing Gong
Wuhan Union Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-2114-7514
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Revision
Version 1
Posted 10 Mar, 2021
No community comments so far
Editorial decision: Major Revisions Needed
On 29 Mar, 2021
Review #? received
Received 06 Mar, 2021
Reviewers invited
Invitations sent on 05 Mar, 2021
Editor assigned
On 22 Feb, 2021
First submitted
On 21 Feb, 2021
Subject Areas
Oncology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Lung cancer is the most commonly diagnosed cancer with a high mortality rate. Cisplatin is one of the most important chemotherapeutic agents for the treatment of lung cancer patients, especially in advanced stages. Recent studies showed that cisplatin may interact with mitochondria which may partly account for its cytotoxicity. In the study, we explored the effect of resistin on cisplatin-induced cytotoxicity in A549 cells and assessed whether mitochondria-dependent apoptosis was involved. Our results found that 25 ng/ml resistin could significantly increase cisplatin-induced apoptosis and G2/M phase arrest, enhance reactive oxygen species generation, exacerbate the collapse of mitochondrial membrane potential, promote the distribution of cytochrome C in the cytoplasm from mitochondria, and activate caspase 3. Therefore, the results suggested that resistin might increase cisplatin-induced cytotoxicity via a mitochondria-mediated pathway in A549 cells. However, the precise mechanism has yet to be explored in the future.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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