Establishment of cancer cell lines from rat hepatocholangiocarcinoma and assessment of the role of granulocyte-colony stimulating factor and hepatocyte growth factor in their growth, motility and survival

Abstract

Background/Aims-Oval cells (OCs), putative hepatic stem cells, may give rise to liver cancers. We developed a carcinogenesis regimen, based upon induction of OC proliferation prior to carcinogen exposure. In our model, rats subjected to 2-acetylaminofluorene/partial-hepatectomy followed by aflatoxin injection (APA regimen) developed well-differentiated hepatocholangiocarcinomas. The aim of this study was to establish and characterize cancer cell lines from this animal model.

Lung Metastasis Fails in MMTV-PyMT Oncomice Lacking S100A4 Due to a T-Cell Deficiency in Primary Tumors

“…G-CSF stimulated skin tumor progression and bone tumor growth (39)(40)(41). G-CSF production increased invasiveness of human head and neck carcinoma and hepatocarcinoma cell lines (42). Interestingly, G-CSF mediates mobilization of CD11b + Gr-1 + myeloid cells that, as it was shown recently, stimulate metastatic spread of tumor (43,44).…”

Heterozygosity for the alpha1-antitrypsin Z allele may confer genetic risk of cholangiocarcinoma

“…In the study by Zhou et al. 6 heterozygosity for the Z allele has been linked to intrahepatic CCA, presumedly arising from bipotent periportal progenitor cells considered to represent a nidus for biphasic primary liver cancers and/or subsets of intrahepatic CCA 13 . In our dataset, we were not able to replicate this observation, although given the confined number of intrahepatic CCAs, comprising no more than 41 cases, our study is underpowered to be confident in refuting this association (potential type II error).…”

Primary isolated hepatic oval cells maintain progenitor cell phenotypes after two-year prolonged cultivation

“…Based on these results, it is suspected that hepatic oval cells will not spontaneously maltransform into cancer-initiating cells; however, environmental factors, such as viruses, carcinogens, and fibrosis factors, might trigger malignant transformation of these cells. Recently, Piscaglia et al [24] found that rats treated only with 2-acetylaminofluorene/partial-hepatectomy did not develop liver cancers, and activation of the oval cell compartment followed by aflatoxin-B1 exposure appears to be critical for hepatocellular carcinoma/cholangiocarcinoma development. These facts support the notion that hepatic progenitors do not spontaneously maltransform, but can be induced to become cancer-initiating cells by exposure to oncogenic factors or reagents.…”