125I seed irradiation could block the migration, proliferation, and invasion of cholangiocarcinoma (CCA) cells, according to a new study published in the journal Dose Response. It can also promote apoptosis through the inactivation of the AKT/VEGFR2/PI3K signaling pathway.

These findings suggest that 125I seed irradiation could serve as an effective therapeutic approach for patients with CCA, but further clinical studies are needed, the researchers noted.

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For the present study, a team of researchers investigated the potential mechanisms of 125I seed irradiation on inactivating the VEGFR2/PI3K/AKT pathway in CCA using 2 human CCA cell lines and an immunoidesficient mouse model.

They found that the invasion, proliferation, and migration of CCA cells irradiated with .6 mCi and .8 mCi 125I seed was inhibited compared to controls. 

Moreover, 125I seed irradiation promoted apoptosis and decreased the expression of PI3K, Bcl-2 proteins, p-VEGFR2, CDK1, VEGFR2, p-AKT/AKT, cyclin B1, and cyclin A. 

The researchers reported similar results with the mouse model. 

When VEGF was overexpressed, the inhibitory effect of .8 mCi 125I seed irradiation was reversed on CCA cell lines suggesting that 125I seed irradiation may promote apoptosis by inactivating the PI3K/VEGFR2/AKT signaling pathway.

CCA is a heterogeneous group of rare malignant tumors originating from the cells of the biliary tree in the liver. The incidence and mortality rate of CCA has been increasing in recent years.

Therapeutic approaches for CCA include radiotherapy, chemotherapy, and targeted therapy. 125I seed implantation has become an effective method for the treatment of many tumors in recent years, including CCA. The main antitumor mechanism of the approach is to promote apoptosis and inhibit the proliferation of cancer cells. 


Luo J, Zheng J, Yao H, et al. Radioactive 125I seed inhibits cell migration and invasion and promotes apoptosis by inactivating the VEGFR2 signaling pathway in cholangiocarcinoma. Dose Response. Published online July 1, 2023. doi:10.1177/15593258231187348