| Background & Purpose:Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide. Portal vein tumor thrombosis (PVTT) is a remarkable characteristic of HCC, and approximately 40.5-90% of advanced HCC has been found to accompany PVTT, which is highly associated with the poor progression. Increasing evidence has shown that radiotherapy has satisfactory curative effect for PVTT in clinic, but the biology behavior changes of PVTT after radiation is still unclear, so we study the radiosensitivity of PVTT and the change of the biology behaviors, in order to better guide clinical practice.Methods:We researched the radiation biology parameters, the biology behavior changes including apoptosis, proliferation and migration and related mechanisms in vitro through compared PVTT-originated cells CSQT-2 with the human liver cell line HL-7702, the human HCC cell lines, Hep3B and Huh7, and we further assessed the radiosensitivity in vivo xenograft.Results:The radiation biology parameters of CSQT-2 cells was smaller than HCC cells. CSQT-2 cells undergone radiation performed higher percentage of apoptotic and death by activated the apoptotic protein caspase3 and PARP, performed more obvious proliferation inhibition by arrested cell cycle in G2/M phase, and decreased PCNA expression, moreover, the migration capacity was weaken. Importantly, radiation induced higher shrinkage rate of xenograft tumor derived from CSQT-2 cells.Conclusions:Our results demonstrated that PVTT-originated cells was more radiosensitive than HCC cells both in vitro and vivo, which provides a basis for clinical application of radiotherapy for HCC with PVTT patients.Potential applications and novelty:Our results firstly demonstrated that PVTT-originated cells were more radiosensitive than HCC cells both in vitro and vivo, firstly unveiled the radiation biology parameters, the biology behavior changes and related mechanisms of PVTT-originated cells, which provides a basis for further study the radiotherapy of PVTT. |
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