PDPN+ cancer‐associated fibroblasts enhance gastric cancer angiogenesis via AKT/NF‐κB activation and the CCL2‐ACKR1 axis
2025

How Cancer-Associated Fibroblasts Help Gastric Cancer Grow

Sample size: 400 publication 10 minutes Evidence: high

Author Information

Author(s): Zhao Zhenxiong, Sun Hui, Liu Yingxue, Zhang Yanqiu, Wang Xin, Wang Xu, Tan Cong, Ni Shujuan, Weng Weiwei, Zhang Meng, Wang Lei, Huang Dan, Gu Wenchao, Chang Jinjia, Sheng Weiqi, Xu Mi-die

Primary Institution: Fudan University Shanghai Cancer Center

Hypothesis

Do PDPN+ cancer-associated fibroblasts enhance angiogenesis in gastric cancer through the AKT/NF-κB signaling pathway?

Conclusion

PDPN+ cancer-associated fibroblasts promote angiogenesis in gastric cancer by secreting CCL2, which activates the PI3K/AKT signaling pathway in endothelial cells.

Supporting Evidence

  • PDPN+ CAFs were found to enhance the migration and tube formation of endothelial cells.
  • High levels of PDPN, CD31, and CCL2 in gastric cancer tissues were associated with poor patient prognosis.
  • CCL2 secreted by PDPN+ CAFs activates the PI3K/AKT signaling pathway in endothelial cells.

Takeaway

Some cells in tumors, called cancer-associated fibroblasts, help cancer grow by making a special chemical that helps blood vessels form, which is important for the tumor's food supply.

Methodology

The study involved analyzing clinical samples, performing immunohistochemical staining, and conducting in vitro and in vivo experiments to assess the role of PDPN+ CAFs in angiogenesis.

Potential Biases

Potential biases may arise from the selection of patient samples and the interpretation of immunohistochemical results.

Limitations

The study does not fully elucidate the molecular mechanisms by which PDPN activates the PI3K/IKK/NF-κB signaling pathway.

Participant Demographics

The study involved 400 gastric cancer patients and 73 normal tissue samples.

Statistical Information

P-Value

p<0.001

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1002/mco2.70037

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