Cheng-Po Hu

Selective suppression of insulin-induced proliferation of cultured human hepatoma cells by somatostatin.

The effects of somatostatin (SRIF), insulin, and triiodothyronine (T3) on the growth of human hepatoma cells were investigated on the well-differentiated human hepatoma cell line Hep3B. Results showed that both insulin and T3 can stimulate cell growth of serum starved Hep3B cells at physiological concentrations. SRIF alone showed little growth-promoting activity. When added concurrently with insulin, however, SRIF suppressed the insulin-induced cell proliferation in a dose-dependent manner. On the other hand, SRIF had no inhibitory effect on T3-induced cell proliferation. SRIF is labile in the medium, with a half-life of about 2 h during culture incubation. SRIF did not disturb the insulin binding to its surface receptors nor inhibit the insulin-dependent receptor kinase activity of Hep3B cells in vitro. These results suggest that postreceptor regulation may be involved. The selective suppression by SRIF of insulin-induced cell growth provides an unique approach to the study of insulin actions on proliferation of human hepatoma cells.

Expression of c-myc gene in human hepatoma

The level of c-myc transcript was examined in liver samples from seven hepatoma patients. Transcripts were detected in all the normal liver parts examined; in contrast, in two hepatoma parts, there was a dramatic reduction in c-myc transcripts. The restriction enzyme pattern of c-myc gene appeared the same among samples. The data suggest that c-myc gene expression might not be required for the maintenance of the tumor state in human liver carcinogenesis.

No association of cytokine gene polymorphisms in Chinese patients with atopic dermatitis

Background.  Atopic dermatitis (AD) is a common chronically relapsing skin disease associated with the activation of T‐helper 2 cells. Recent studies have shown that polymorphisms in the genes for interleukin (IL)‐4, the IL‐4 receptor, IL‐13, and signal transducer and activator 6 (STAT6) may contribute to susceptibility of AD. To date, no cytokine gene polymorphism study has been conducted on Chinese patients with AD.

Expression of Multiple Oncogenes in Human Esophageal Carcinomas

To study the oncogenesis of human esophageal carcinoma, the expression of a variety of oncogenes was studied in 10 esophageal carcinoma cell lines and 16 pairs of tumor and nontumor tissues removed from patients with esophageal carcinoma. Northern blot analyses using 11 different oncogene probes revealed that 5 oncogenes, i.e. c-myc, c-H-ras, c-sis, c-raf, and c-fos, were expressed. Among them, a variant c-sis mRNA transcript of 2.7 kilobase (kb) was expressed in 7 of 10 cell lines and in 9 of 16 tumor tissues. Furthermore, an overexpression and an amplification of c-myc gene was observed in some cell lines. These results suggest that multiple oncogene expression may be required for the induction, maintenance, and progression of esophageal carcinoma. The expression of a 2.7-kb transcript, of c-sis and overexpression of c-myc gene may play some role in the carcinogenesis of esophageal carcinoma.

Effects of Scutellaria baicalensis Georgi on Macrophage-Hepatocyte Interaction Through Cytokines Related to Growth Control of Murine Hepatocytes

The aim of this study is to elucidate the effects of Scutellaria baicalensis Georgi (SbG) extract and its constituents on macrophage-hepatocyte interaction in primary cultures. By using trans-well primary Kupffer cell culture or conditioned medium (CM) from murine macrophage RAW264.7 cell line (RAW cells), effects of SbG on hepatocyte growth were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide and trypan blue exclusion assay. Cytokine production, antibody-neutralization studies, and molecular mechanisms of transforming growth factor (TGF)-β1 gene expression were elucidated on SbG-treated RAW264.7 cells. In addition, recombinant human TGF-β1 (r-human TGF-β1) was added to elucidate the mechanisms of SbG effects on cultured hepatocytes. Immunohistochemistry using anti-NF-κB antibody was used to determine the possible signal transduction pathways in primary hepatocyte culture. The results showed that SbG stimulated the proliferation of cultured hepatocytes, possibly through NF-κB, but not of Toll-like receptor 4 activation; whereas SbG-RAW-CM and SbG in trans-well significantly suppressed the proliferation of hepatocytes. Antibody-neutralization studies revealed that TGF-β1 was the main antimitotic cytokine in SbG-treated RAW cells CM. The growth stimulation effect of SbG on cultured hepatocytes was inhibited by exogenous administration of r-human TGF-β1. Furthermore, SbG induced NF-κB translocation into the nuclei of cultured cells. In the RAW264.7 line, SbG and baicalin stimulated TGF-β1 gene expression via NF-κB and protein kinase C activation. We conclude that SbG stimulates hepatocyte growth via activation of the NF-κB pathway and induces TGF-β1 gene expression through the Kupffer cell–hepatocyte interaction, which subsequently results in the inhibition of SbG-stimulated hepatocyte growth.