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CT1 Cytotoxic Effects Against MDA-MB-231 Evasion

Breast cancer is the most commonly occurring cancer worldwide, more than 2.26 million new cases occurred in women in 2020. Treatment for breast cancer is normally individualized to the patient based on the presence of different receptors, these receptors include HER2, progesterone, and estrogen. The presence of these receptors generally comes with an amenable prognosis, and a wide array of available treatments. There are types of breast cancers that do not have any of these receptors and tend to be much more aggressive. This type of cancer is called triple negative and represents about 10 percent of all breast cancer occurrences in the United States. The lack of receptors makes this type of cancer extremely difficult to treat and generally comes with a poor prognosis. In the present study, we used triple negative breast cancer cell line MDA-MB231, which is known to use actin remodeling to evade immunologic response. These cells were treated with two novel, structurally similar flavonoids, CT1 and CT3 derived from an ethnobotanically recognized species of Chromolaena.
CT1 and CT3 are extracted from the leaves of Chromolaena tacotana and then isolated and purified by chromatography. These compounds are used to treat cancer cells, at different concentrations that include 5, 10, 20, 40 and 80mM. MTT assays are used to determine their effect on cell viability, and the mechanism of action was analyzed by immunoblotting and TUNEL..
CT1 has a significantly stronger inhibitory effect on MDA-MB231 cell viability as compared to CT3. Preliminary analysis of the mechanism of action of CT1 has revealed that it neither follows the canonical intrinsic apoptotic pathway nor the extrinsic pathway that involves the activated form of c-JUN.
By up-regulating actin, triple negative breast cancer is able to evade immunologic response and cancer treatment. CT1, a novel flavonoid extracted from the leaves of Chromoleana tacotana has shown cytotoxic effects against triple negative breast cancer cells effectively bypassing the actin response. The mechanism of action is currently under study.

Identiferoai:union.ndltd.org:ETSU/oai:dc.etsu.edu:asrf-2181
Date25 April 2023
CreatorsHarding, Jeanna, Locke, Autumn, Akinbote, Olasunkanmi, Torrenegra, Ruben, Hagood, Kendra, Hackworth, Keagan, Palau, Victoria
PublisherDigital Commons @ East Tennessee State University
Source SetsEast Tennessee State University
Detected LanguageEnglish
Typetext
SourceAppalachian Student Research Forum

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