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Morusin Suppresses Pancreatic Cancer Cell Proliferation and Migration by Targeting SLC6A12 to Inhibit NF-κB and
Wenyan Yang1,2, Wei Zhu3, Zhiyang Yao1,2
1College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou, Zhejiang, 310014, China.
Introduction:
Pancreatic cancer is characterized by a poor prognosis and low survival rate, underscoring the urgent need for the development and optimization of novel therapeutic interventions. Morusin has been reported to have anticancer activity in a variety of cancers. Therefore, the present study aimed to elucidate the anticancer effects and potential mechanisms of Morusin in pancreatic cancer.
Methods:
We evaluated the anticancer effect of Morusin in pancreatic cancer cells, including its impact on pancreatic cancer cell proliferation, colony formation potential, migration, invasion, cell cycle and apoptosis. RNA sequencing (RNA-seq) analysis was employed to identify potential genes involved in the anticancer activity of Morusin. Furthermore, RT-qPCR and Western blot analysis were utilized to verify the findings.
Results:
Our results demonstrated that Morusin administration significantly impaired cell proliferation, migration and invasive activity of pancreatic cancer cells. Additionally, Morusin induced apoptosis and disrupted cell cycle progression. Importantly, Morusin was found to co-regulate SLC6A12, HSPA2, P2RY6 and JPH2 in both cell lines by RNA-seq analysis, with the most significant decrease in mRNA levels of SLC6A12 following administration. Mechanistically, Morusin was found to regulate the expression of SLC6A12 and inhibit NF-κB and β-catenin signaling pathways, which may represent the underlying mechanisms of its antitumor activity.
Conclusion:
Our findings suggest that Morusin holds potential as an anti-pancreatic cancer agent by targeting SLC6A12 and modulating its associated signaling pathways.
Insights
Morusin demonstrates significant anticancer effects against pancreatic cancer by inhibiting cell proliferation, migration, and invasion. It also induces apoptosis and targets SLC6A12, offering potential as a novel therapeutic agent.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Pancreatic cancer has a poor prognosis, necessitating new therapeutic strategies.
- Morusin exhibits known anticancer properties across various cancer types.
- This study investigates Morusin's efficacy and mechanisms in pancreatic cancer.
Purpose of the Study:
- To evaluate the anticancer effects of Morusin on pancreatic cancer cells.
- To elucidate the molecular mechanisms underlying Morusin's anti-pancreatic cancer activity.
- To identify potential therapeutic targets for Morusin in pancreatic cancer treatment.
Main Methods:
- Assessed Morusin's impact on pancreatic cancer cell proliferation, colony formation, migration, and invasion.
- Analyzed cell cycle progression and apoptosis induction following Morusin treatment.
- Utilized RNA sequencing (RNA-seq), RT-qPCR, and Western blot to identify and verify key genes and pathways.
Main Results:
- Morusin significantly inhibited pancreatic cancer cell proliferation, migration, and invasion.
- Morusin induced apoptosis and disrupted cell cycle progression in pancreatic cancer cells.
- Morusin modulated SLC6A12 expression and inhibited NF-κB and β-catenin signaling pathways.
Conclusions:
- Morusin exhibits potent anti-pancreatic cancer activity.
- Targeting SLC6A12 and associated signaling pathways are key mechanisms of Morusin's action.
- Morusin shows promise as a potential therapeutic agent for pancreatic cancer.
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