PLK1 OVEREXPRESSION POST-INCOMPLETE ABLATION AMPLIFIES RESIDUAL HCC PROLIFERATION AND INVASION

TAT, a widely used treatment for Hepatocellular carcinoma (HCC), can exacerbate the progression of residual HCC. The present study investigated the mechanism of action of PLK1 following Incomplete Thermal Ablation (ITA) of HCC. PLK1 levels in HCC were determined using quantitative real-time polymerase chain reaction (qRT-PCR) from clinical patient samples, immunohistochemistry (IHC) from tissue microarray, and data from globally high-throughput data and microarrays. The PLK1 levels and their effect on the biological phenotype of heat-stress HCC cells were evaluated through in vitro experiments. We detected PLK1 abnormal expression in HCC models of nude mice subjected to ITA. We detected the effects of different PLK1 expression levels on epithelial-mesenchymal transition (EMT) pathway proteins. PLK1 exhibited an overexpression in HCC tissues with a standardized mean difference (SMD) of 1.19 (3414 HCC and 3036 non-HCC tissues were included), distinguishing HCC from non-HCC effectively (area under the curve (AUC)=0.9). The qRT- PCR data from clinical HCC patient samples and IHC from HCC tissue microarray results also indicated an overexpressed level. In the incomplete ablation models, an increased PLK1 expression was found in both heat-stress cells and subcutaneous tumors. The upregulation of PLK1 following ITA was found to enhance the malignancy of HCC and exacerbate the proliferation, migration, and invasion of residual HCC cells, whereas PLK1 knockdown suppressed the biological malignancy of HCC cells. Meanwhile, PLK1 has different regulatory effects on various EMT pathway proteins. PLK1 promotes the progression of residual HCC by activating the EMT pathway after ITA, which might provide a novel idea for the treatment and prognosis of residual HCC.