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Anticancer Activity of Iso-Mukaadial Acetate on Pancreatic and Colon Cancer Cells
Portia Raphela-Choma1, Lesetja Motadi1, Mthokosizi Simelane1
1Department of Biochemistry, University of Johannesburg, Corner Kingsway and University Road, Auckland Park, Johannesburg, 2092, South Africa.
Background:
Pancreatic cancer and colon cancer pose significant challenges in treatment, with poor prognoses. Natural products have long been explored for their potential as anticancer agents. Iso-mukaadial acetate has shown promise in inducing apoptosis in breast and ovarian cancer cells. The objective of this study was to investigate the effect of Iso-mukaadial acetate on pancreatic (MIA-PACA2) and colon (HT29) cancer cell lines.
Methods:
Pancreatic (MIA-PACA2) cancer cells, colon (HT29) cancer cells, normal embryonic kidney cells (HEK 293), and normal lung cells (MRC5) were cultured and treated with Iso-mukaadial acetate (IMA) for 24 hours. The viability assays were conducted using Alamarblue reagent and a real-time cell viability monitoring system, xCELLigence. The IC50 values were determined, followed by assessments of ATP production, caspase 3/7 activation, mitochondrial function, morphological changes using a light microscope, and gene expression changes via RT-PCR.
Results:
This study indicates that Iso-mukaadial acetate exhibited concentration-dependent cytotoxic effects, slowing cellular proliferation in both cancer cell lines. Activation of the mitochondrial apoptotic pathway and caspase 3/7 suggests induction of apoptosis. Reduced ATP production and altered gene expression further support its anticancer properties. Morphological changes after treatment with Iso-mukaadial acetate showed apoptotic characteristics which may suggest that apoptosis was induced.
Conclusions:
According to the results obtained, Iso-mukaadial acetate shows potential as an anticancer agent, evidenced by its effects on cellular viability, mitochondrial function, ATP production, caspase activation, and gene expression in pancreatic and colon cancer cells. These findings highlight its promise for further investigation and potential in the development of therapeutic agents.
Insights
Iso-mukaadial acetate demonstrates anticancer potential by inhibiting pancreatic and colon cancer cell proliferation. It induces apoptosis through mitochondrial pathways and caspase activation, supporting its development as a therapeutic agent.
Area of Science:
- Natural product chemistry
- Cancer biology
- Molecular pharmacology
Background:
- Pancreatic and colon cancers present significant therapeutic challenges with poor prognoses.
- Natural products are a key area of research for novel anticancer agents.
- Iso-mukaadial acetate has previously shown promise in inducing apoptosis in breast and ovarian cancer cells.
Purpose of the Study:
- To investigate the anticancer effects of Iso-mukaadial acetate on pancreatic (MIA-PACA2) and colon (HT29) cancer cell lines.
- To evaluate the impact of Iso-mukaadial acetate on cancer cell viability, proliferation, and apoptosis.
Main Methods:
- Cell culture of pancreatic (MIA-PACA2), colon (HT29), and normal cell lines (HEK 293, MRC5).
- Treatment with Iso-mukaadial acetate (IMA) and assessment of cell viability using Alamarblue and xCELLigence.
- Analysis of ATP production, caspase 3/7 activation, mitochondrial function, and gene expression (RT-PCR).
Main Results:
- Iso-mukaadial acetate exhibited concentration-dependent cytotoxic effects, reducing proliferation in both cancer cell lines.
- Evidence of apoptosis induction via mitochondrial pathway activation and caspase 3/7 activity.
- Reduced ATP production, altered gene expression, and characteristic morphological changes supported the anticancer properties.
Conclusions:
- Iso-mukaadial acetate shows significant potential as an anticancer agent against pancreatic and colon cancer.
- Its mechanism involves inducing apoptosis, affecting cellular viability, mitochondrial function, and gene expression.
- Further research into Iso-mukaadial acetate is warranted for potential therapeutic development.
