Metabolic and physiological pathways are overall suppressed during hibernationSuppressed fat catabolism with active CPT1A suggests a unique energysaving strategy

The objective of this study is to evaluate the efficacy of radiotherapy for the treatment of arteriovenous shunting (AVS) in patients with hepatocellular carcinoma (HCC). Between November 1997 and April 2005, 20 HCC patients with AVS were referred to our department for radiotherapy. The radiation was delivered with 10-15 MV X-ray given 5 days per week at 2 approximately 2.5 Gy per fraction. Total doses ranged from 45 to 64 Gy (median dose 60 Gy). The patients were followed up with color Doppler sonography. When non-invasive imaging suggested obliteration, X-ray angiography was performed to verify the results. Four of the 20 AVS proved to be completely obliterated at X-ray angiography in 1.9, 2.8, 1.8 and 2.9 months after radiotherapy. One of the remaining 16 showed obvious regression on Doppler sonography 0.5 months after radiotherapy, but X-ray angiography was not performed to verify the result. Radiation-related hepatic failure did not occur during the follow-up period. In conclusion, radiotherapy is a treatment alternative for AVS in HCC patients and gives patients with poor prognosis the chance to receive further transcatheter arterial embolization.

Background: Hepatocellular carcinoma (HCC) is the most common malignant tumor of the adult liver, exhibiting rapid progression and poor prognosis. Chlorogenic acid (CGA), a polyphenol, has several biological activities, including the suppression of liver cancer cell invasion and metastasis. Increased levels or alterations in the function of DNMT1 are associated with the inactivation of tumor suppressor genes. However, the CGA-affected DNMT1 expression mediated mechanism is still unclear. Methods: The human hepatocellular carcinoma (HCC) HepG2 cells were treated with a positive control drug (5-AZA) or varying doses of CGA. DNA methyltransferase 1 (DNMT1) protein levels and other relevant proteins were evaluated using Western blotting and immunocytochemistry. Cell-cycle analysis was performed by flow cytometry-based PI staining, and cell viability was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide (MTT) assay. The transwell invasion and wound healing assays were used to evaluate cell migration and invasion. In vivo proliferation of the HCC cells was detected. We investigated the expression of DNMT1, p53, p21, pERK , MMP-2, and MMP-9 in tumors using immunohistochemical analysis. Results: Our results showed that CGA inhibited the proliferation, colony formation, invasion, and metastasis of HepG2 cells both in vitro and in vivo by down-regulating DNMT1 protein expression, which enhanced p53 and p21 activity, and resulting in a significant reduction in cell proliferation and metastasis. Moreover, CGA inactivated ERK1/ 2 and reduced MMP-2 and MMP-9 expression in HepG2 cells. Conclusions: CGA can suppress liver cancer cell proliferation, invasion, and metastasis through several pathways. CGA could serve as a candidate chemopreventive agent for HCC.

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