Cytotoxic and apoptotic effect of chalcone 5 on mouse colon cancer cells CT-26
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Title |
Cytotoxic and apoptotic effect of chalcone 5 on mouse colon cancer cells CT-26
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Creator |
Ristić, Tijana
Luković, Jovan Nikolić, Ivana Anđelković, Marija Pirković, Marijana Stanojević Canović, Petar Muškinja, Jovana Popović, Suzana Mitrović, Marina |
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Subject |
Apoptosis
Cell death Cell line Chalcones Colon cancer Mouse cell line |
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Description |
145-152
According to World Health Organization data, various forms of cancer cause around 10 million deaths each year. Nearly 2 million new colon and rectal cancer cases were detected in 2020, making it the second greatest cause of cancer death. Aside from the harmful effects of various chemotherapeutic agents, a special difficulty for treating and eradicating these diseases is tumor resistance to existing anticancer medications and undesired side effects of chemotherapy against healthy cells and tissue. Chalcones are precursors for the synthesis of flavonoids and other compounds with a heterocyclic structure. The biological activities of this category of chemicals include antibacterial, anti-inflammatory, anticancer, antidiabetic, and antiproliferative properties. In the current study, we therefore examined the antitumor and apoptotic effects of chalcone 5 on mouse colon carcinoma cell line CT-26. Chalcone 5 caused the inner mitochondrial apoptotic pathway to be triggered in CT-26 cells by inducing apoptosis, disrupting the potential of the mitochondrial membrane and causing the release of cytochrome c into the cytosol. Based on results obtained in this study, chalcone 5 may be recommended as a potential promising anti-cancer candidate for future in vivo research studies utilizing experimental animals. |
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Date |
2024-02-21T06:58:44Z
2024-02-21T06:58:44Z 2024-02 |
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Type |
Article
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Identifier |
0975-0959 (Online); 0301-1208 (Print)
http://nopr.niscpr.res.in/handle/123456789/63367 https://doi.org/10.56042/ijbb.v61i3.4446 |
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Language |
en
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Publisher |
NIScPR-CSIR,India
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Source |
IJBB Vol.61(03) [March 2024]
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