Abstract
Portal vein occlusion increases the resectability of initially unresectable liver cancer by inducing hypertrophy in non-occluded liver lobes. However, the mechanisms of how portal vein occlusion induces hepatic hypertrophy remain unclear. A cDNA microarray was used to identify the gene expression signatures of ligated (LLLs) and nonligated liver lobes (NLLLs) at different time points after portal vein ligation (PVL). The results of a bioinformatics analysis revealed that LLLs and NLLLs displayed different gene expression profiles. Moreover, the expression levels of both coding and noncoding RNA were different between LLLs and NLLLs at different time points after PVL. A series test of cluster analysis revealed that the No. 22 and No. 5 expression patterns, which showed altered expression at 24 h and maintained this altered expression over the following 14 days, had the lowest P values and the highest number of differentially expressed genes in both the LLLs and NLLLs. The results of a GO analysis showed the activation of hypoxia pathways in LLLs and the activation of cell proliferation and cell-cycle pathways in NLLLs, suggesting the involvement of these pathways in PVL-induced hepatic hypertrophy and regeneration. These results provide insight into the molecular mechanisms underlying hepatic hypertrophy and regeneration induced by portal vein occlusion, and they identify potential targeting pathways that can promote the clinical application of PVL in liver cancer therapy.
Highlights
Complete hepatic tumor resection is the main option for curative treatment of liver malignancies and provides patients with a chance for long-term survival (Utsunomiya et al 2014)
Similar results were obtained when the NLLLM/WLM and LLLM/WLM ratios were analyzed (Fig. 1C). These results indicated that portal vein ligation (PVL) induced hypertrophy in nonligated liver lobes (NLLLs) and atrophy in ligated liver lobes (LLLs) in rats
The results showed that genes in profile No 22 from LLLs were significantly enriched in gene transcription, regulation, and response to hypoxia for biological processes (BP); DNA and protein binding for molecular function (MF); and the cytoplasm and nucleus for cell components (CC) (Table 2)
Summary
Complete hepatic tumor resection is the main option for curative treatment of liver malignancies and provides patients with a chance for long-term survival (Utsunomiya et al 2014). Portal vein occlusion via embolization (PVE) or ligation (PVL) induces hypertrophy in non-occluded liver lobes and increases the resectability of an inadequate functional remnant liver volume (Siriwardana et al 2012). The mechanisms of how PVE/PVL induces contralateral hepatic hypertrophy are still poorly understood. PVE has been reported to induce apoptosis in the embolized lobe and proliferation in the non-embolized lobe, which may involve the altered expression of transforming growth factor-alpha (TGF-␣) and transforming growth factor-beta (TGF-) in livers after PVE (Kusaka et al 2006). Changes in portal flow and cytokine expression after PVE/PVL were reported in animal models. A reduction in left liver flow and an increase in right liver flow were observed when left portal vein stenosis was performed — results that were further verified by the dilation of the portal branches in the non-
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