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Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
Published on: April 29, 2014
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Paeoniflorin Inhibits Migration- and Invasion-Promoting Capacities of Gastric Cancer Associated Fibroblasts
Zhen-Fei Wang1, Da-Guang Ma1, Ling Wang2
1The Laboratory for Tumor Molecular Diagnosis, Affiliated People's Hospital of Inner Mongolia Medical University, Hohhot, 010020, China.
Chinese Journal of Integrative Medicine
|October 27, 2018
Summary
Paeoniflorin effectively inhibits gastric cancer-associated fibroblast (GCAF) migration and invasion. This compound targets microRNA-149 and IL-6, offering potential as a novel therapeutic agent for the cancer microenvironment.
Area of Science:
- Oncology
- Cell Biology
- Pharmacology
Background:
- Gastric cancer-associated fibroblasts (GCAFs) promote tumor cell migration and invasion.
- The role of GCAFs in the tumor microenvironment requires further investigation for therapeutic targeting.
Purpose of the Study:
- To evaluate the inhibitory effects of paeoniflorin on GCAF-mediated migration and invasion.
- To elucidate the molecular mechanisms by which paeoniflorin exerts its effects on GCAFs.
Main Methods:
- GCAFs and normal fibroblasts (GNFs) were cultured and treated with paeoniflorin.
- AGS gastric cancer cells were cultured in conditioned media from treated fibroblasts.
- Cell migration, invasion, IL-6, microRNA-149, STAT3, and MMP9 levels were assessed.
Main Results:
- GCAFs significantly enhanced AGS cell migration and invasion compared to GNFs.
- Paeoniflorin treatment inhibited GCAF-induced migration and invasion.
- Paeoniflorin suppressed IL-6 production and secretion by upregulating microRNA-149 in GCAFs, thereby inhibiting IL-6-STAT3-MMP signaling in AGS cells.
Conclusions:
- Paeoniflorin inhibits GCAF-mediated cancer cell migration and invasion.
- The mechanism involves targeting microRNA-149 and IL-6, disrupting the IL-6-STAT3-MMP pathway.
- Paeoniflorin shows promise as a therapeutic agent for targeting the cancer microenvironment.
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