CXCR4/TGF-β1 mediated hepatic stellate cells differentiation into carcinoma-associated fibroblasts and promoted liver metastasis of colon cancer.

: Liver metastasis of colon cancer is strongly affected by the tumor microenvironment (TME), with interactions between tumor cells and cancer-associated fibroblasts (CAFs) in particular. TGF-β is well known for its ability to mediate the CAF phenotype, and CXCR4 expression is closely correlated to poor prognosis in CRC. The relationship between these two signaling pathways remains to be delineated in liver metastasis of colon cancer.

CXCR4/TGF-β1 mediated self-differentiation of human mesenchymal stem cells to carcinoma-associated fibroblasts and promoted colorectal carcinoma development.

: Tumor microenvironment (TME) is a crucial part of tumor hallmarks. Mesenchymal stem cells (MSCs), important components of TME, are the main source of Carcinoma-associated fibroblasts (CAFs), but the mechanism of transformation regulation is still unclear. Transforming growth factor-β1 (TGF-β1), chemokine Stromal cell-derived factor-1 (SDF-1) and its endogenous receptor CXCR4 may play important roles during this process.

TGFβ1 is essential for MSCs-CAFs differentiation and promotes HCT116 cells migration and invasion via JAK/STAT3 signaling.

Background And Purpose: Colorectal cancer (CRC) frequently metastasizes to the liver, which involves the participation of multiple cytokines. Tumor microenvironment (TME) composed of cancer-associated fibroblasts (CAFs) and tumor cells acts as an essential factor in cancer metastasis. Transforming growth factor β1 (TGFβ1) is a vital cytokine involved in migration and invasion of cancer cells.

FAK is involved in invasion and metastasis of hepatocellular carcinoma.

Studies have shown that focal adhesion kinase (FAK) is overexpressed in several human tumors and plays an important role in tumor progression. However, the role and underlying mechanisms of FAK in hepatocellular carcinoma (HCC) progression remains to be elucidated. In this study, we examined FAK and phosphorylated FAK Tyr397 expression in a large series of HCCs.

Clinical significance of miR-221 and its inverse correlation with p27Kip¹ in hepatocellular carcinoma.

The aim of the present study is to explore possible role of miR-221 in the pathogenesis of HCC. Matched HCC and adjacent non-cancerous samples were assayed for the expression of miR-221 and three G1/S transition inhibitors: p27(Kip1), p21(WAF1/Cip1)and TGF-β1 by in situ hybridization and immunohistochemistry respectively. p27(Kip1) is one of miR-221's proven targets.

MicroRNA-9 reduces cell invasion and E-cadherin secretion in SK-Hep-1 cell.

MicroRNAs (miRNAs) are an abundant class of short noncoding RNAs that can posttranscriptionally regulate gene expression in animals. They are also involved in cancer initiation and progression, and their expression profiles serve as phenotypic signatures of different cancers. The roles played by microRNAs specifically in "micromanagement of metastasis" has been addressed only recently.

Bead-based microarray analysis of microRNA expression in hepatocellular carcinoma: miR-338 is downregulated.

Aim: Recent studies have underlined causative links between microRNA (miRNA) deregulation and cancer development. However, the relevance of abnormally expressed miRNA to tumor biology has not been well understood in hepatocellular carcinoma (HCC).

Methods: A bead-based miRNA expression profiling method was performed on 20 pairs of surgically removed HCC and adjacent non-tumorous tissue (NT).

[Effect of recipient derived bone marrow stromal cells on immunological rejection in mouse allogeneic skin transplantation].

Objective: To investigate the effect of recipient derived bone marrow stromal cells (BMSCs) on immunological rejection in mouse allogeneic skin transplantation.

Methods: The C57BL/6 to BALB/c allogeneic skin transplantation model was created. The bone marrow stromal cells (BMSCs) were isolated from BALB/c by gradient density centrifugation and adhesion separation.

Involvement of PI3K/PTEN/AKT/mTOR pathway in invasion and metastasis in hepatocellular carcinoma: Association with MMP-9.

Aim: To investigate the status of Phosphatidylinositol 3-kinase (PI3K)/PTEN/AKT/mammalian target of rapamycin (mTOR) pathway and its correlation with clinicopathological features and matrix metalloproteinase-2, -9 (MMP-2, 9) in human hepatocellular carcinoma (HCC).

Methods: PTEN, Phosphorylated AKT (p-AKT), Phosphorylated mTOR (p-mTOR), MMP-2, MMP-9 and Ki-67 expression levels were evaluated by immunohistochemistry on tissue microarrays containing 200 HCCs with paired adjacent non-cancerous liver tissues. PTEN, MMP-2 and MMP-9 mRNA levels were determined by real-time RT-PCR in 36 HCCs.

[Epigallocatechin-3-gallate induces apoptosis in human hepatocellular carcinoma cells].

Objective: To investigate the effects of epigallocatechin-3-gallate (EGCG) on human hepatocellular carcinoma (HCC) cells and mechanism thereof.

Method: Human HCC cells of the lines HepG2 and SMMC-7721 were cultured and treated with of EGCG of the concentrations of 6.25, 12.

Expression patterns and polymorphisms of PTCH in Chinese hepatocellular carcinoma patients.

Aberrant activation of Hedgehog signaling pathway leads to pathological consequences in a variety of human tumors. PTCH (PTCH1), the receptor of Hedgehog pathway, is reported to function as a gatekeeper in tumor formation. Here we report, by semi-quantitative RT-PCR, PTCH expression was found in 38 hepatocellular carcinoma (HCC) patients (66%).