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Updated: May 4, 2026
Flow Cytometry-Based Isolation and Therapeutic Evaluation of Tumor-Infiltrating Lymphocytes in a Mouse Model of Pancreatic Cancer
Published on: January 17, 2025
Embelin suppresses pancreatic cancer growth by modulating tumor immune microenvironment
Justine L Marsh1, Chris P Jackman1, Su-Ni Tang2
1Department of Biochemistry, The University of Texas Health Science Center at Tyler, Tyler, Texas 75708.
Abstract:
Since pancreatic carcinoma is largely refractory to conventional therapies, development of novel agents is required for the effective treatment of pancreatic cancer. The objective of this paper was to examine the molecular mechanisms by which embelin inhibited human pancreatic cancer growth in mice by modulating tumor immune microenvironment. Embelin inhibited PANC-1 tumor growth, angiogenesis, and metastasis which were associated with suppression of Akt and Sonic Hedgehog (Shh) pathways. Embelin inhibited the expression of Bcl-2, cyclin D1, CDK2 and CDK6, IL-6 and IL-8, and induced the expression of Bax in tumor tissues. Embelin also reversed epithelial-mesenchymal transition by up-regulating E-cadherin and inhibiting the expression of Snail, Slug and Zeb1. Embelin inhibited pancreatic cancer growth in Kras(G12D) mice by modulating tumor immune microenvironment where CTL, NKT, γδT, NK, and IFNγ (Th1 type) cells were up-regulated, and Th17, PMN-MDSC, IL-6 and IL-8 (Th2 type) immune cells were inhibited. These data suggest that embelin can inhibit pancreatic cancer growth by modulating tumor immune microenvironment and Akt and Shh pathways, and inhibiting inflammation. Embelin may offer therapeutic benefits for the treatment and/or prevention of pancreatic cancer.
Insights
Embelin effectively inhibits pancreatic cancer growth by modulating the tumor immune microenvironment and key molecular pathways. This natural compound shows therapeutic potential for pancreatic cancer treatment and prevention.
Area of Science:
- Oncology
- Immunology
- Pharmacology
Background:
- Pancreatic cancer is notoriously resistant to conventional treatments, necessitating the development of novel therapeutic agents.
- Understanding the molecular mechanisms underlying cancer progression and immune evasion is crucial for effective treatment strategies.
Purpose of the Study:
- To investigate the molecular mechanisms by which embelin inhibits human pancreatic cancer growth in mice.
- To evaluate embelin's effect on the tumor immune microenvironment and its potential therapeutic benefits.
Main Methods:
- Embelin treatment in PANC-1 and Kras(G12D) mouse models of pancreatic cancer.
- Analysis of tumor growth, angiogenesis, metastasis, and molecular markers (Akt, Shh, Bcl-2, Bax, E-cadherin, Snail, Slug, Zeb1).
- Assessment of immune cell populations (CTL, NKT, γδT, NK, Th1, Th17, PMN-MDSC) and cytokine profiles (IFNγ, IL-6, IL-8) within the tumor microenvironment.
Main Results:
- Embelin suppressed PANC-1 tumor growth, angiogenesis, and metastasis by inhibiting Akt and Sonic Hedgehog (Shh) pathways.
- Embelin modulated apoptosis-related proteins (Bcl-2, Bax) and reversed epithelial-mesenchymal transition (EMT).
- In Kras(G12D) mice, embelin enhanced anti-tumor immunity by up-regulating cytotoxic immune cells (CTL, NKT, γδT, NK) and Th1 cytokines, while suppressing pro-tumorigenic Th17 cells and myeloid-derived suppressor cells (PMN-MDSC).
Conclusions:
- Embelin demonstrates significant anti-cancer activity against pancreatic cancer by modulating the tumor immune microenvironment and inhibiting critical signaling pathways (Akt, Shh).
- Embelin's ability to suppress inflammation and promote anti-tumor immunity suggests its potential as a therapeutic agent for pancreatic cancer treatment and prevention.
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