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Pt3R5G inhibits colon cancer cell proliferation through inducing ferroptosis by down-regulating SLC7A11
Lin Han1, Yamei Yan2, Meiyang Fan3
1Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China.
Aims:
Colon cancer (CC) is a prevalent malignancy worldwide and is one of the most easily altered cancers by dietary regulation. Petunidin 3-O-[rhamnopyranosyl-(trans-p-coumaroyl)]-5-O-(β-D-glucopyranoside) (Pt3R5G) isolated and purified from Lycium ruthenicum Murray, which exhibits highly efficient antioxidant activity and specific anticancer effects, is the flavonoids compound. We aimed to study the effect of Pt3R5G on CC cells and elucidate the potential underlying mechanisms.
Main Methods:
Cell proliferation was measured by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and colony formation assays. Cell cycle, cell apoptosis and reactive oxygen species (ROS) analysis were performed by flow cytometry. RNA-sequencing was performed to elucidate the potential underlying mechanisms. The lipid peroxidation level of cells was detected by malondialdehyde (MDA) assay. The mitochondrial morphology of cells was inspected using a transmission electron microscope. Additionally, we overexpressed SLC7A11 to perform rescue experiments. In vivo, xenograft mice assay was performed to verify the effect of Pt3R5G on the growth of colon cancer.
Key Findings:
Pt3R5G reduced the cell activity by blocking the cell cycle in G0/G1 phase, inducing the apoptosis and ferroptosis in RKO cells. The overexpressed of SLC7A11, a significantly down-regulated expression gene caused by Pt3R5G, rescued the cell proliferation inhibition and ferroptosis process. Furthermore, Pt3R5G inhibited tumor growth in nude mice. Our study suggests that Pt3R5G inhibits RKO cell proliferation through mainly reducing ferroptosis by down-regulated SLC7A11.
Significance:
As a potential therapeutic drug, Pt3R5G showed efficient anticancer activity through a variety of pathways.
Insights
Petunidin 3-O-[rhamnopyranosyl-(trans-p-coumaroyl)]-5-O-(β-D-glucopyranoside) (Pt3R5G) inhibits colon cancer cell growth by inducing apoptosis and ferroptosis, primarily by down-regulating SLC7A11. This flavonoid compound demonstrates potential as an anticancer therapeutic.
Area of Science:
- Biochemistry and Molecular Biology
- Cancer Research
- Pharmacology
Background:
- Colon cancer (CC) is a significant global health concern, with dietary factors influencing its progression.
- Flavonoids, such as Petunidin 3-O-[rhamnopyranosyl-(trans-p-coumaroyl)]-5-O-(β-D-glucopyranoside) (Pt3R5G) from Lycium ruthenicum Murray, possess antioxidant and anticancer properties.
- Understanding the mechanisms of novel compounds like Pt3R5G is crucial for developing new CC therapies.
Purpose of the Study:
- To investigate the anti-cancer effects of Pt3R5G on colon cancer cells.
- To elucidate the underlying molecular mechanisms responsible for Pt3R5G's efficacy.
- To evaluate the therapeutic potential of Pt3R5G in preclinical models.
Main Methods:
- Cell viability and proliferation assessed via MTT and colony formation assays.
- Cell cycle, apoptosis, and reactive oxygen species (ROS) analyzed by flow cytometry.
- RNA-sequencing, malondialdehyde (MDA) assay, transmission electron microscopy, and SLC7A11 overexpression rescue experiments were employed.
Main Results:
- Pt3R5G inhibited RKO cell proliferation by arresting the cell cycle at the G0/G1 phase, inducing apoptosis and ferroptosis.
- Down-regulation of SLC7A11 by Pt3R5G was identified as a key mechanism, with its overexpression rescuing proliferation and ferroptosis.
- In vivo studies confirmed that Pt3R5G significantly inhibited tumor growth in a xenograft mouse model.
Conclusions:
- Pt3R5G exhibits potent anticancer activity against colon cancer cells.
- The primary mechanism involves the inhibition of ferroptosis through down-regulation of SLC7A11.
- Pt3R5G represents a promising candidate for further development as a colon cancer therapeutic agent.
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