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Int J Cancer. 2000 Nov 15;88(4):507-18.
Enhancement of metastatic properties of pancreatic cancer cells by MUC1 gene encoding an anti-adhesion molecule.

Satoh S, Hinoda Y, Hayashi T, Burdick MD, Imai K, Hollingsworth MA.

The First Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.

MUC1 mucin expression has been shown to be associated clinicopathologically with metastasis and poor clinical outcome in a variety of tumors. To further investigate this finding experimentally, human pancreatic cancer S2-013 cells overexpressing MUC1 were used for spontaneous metastatic potential in nude mice. It was found that the number of lung metastases of MUC1 transfectants was significantly higher than that of control cells. To analyze the molecular mechanisms that underlie the increased metastatic activity, in vitro adhesion assays were performed. MUC1 mucin expression enhancedin vitro invasiveness and motility of S2-013 cells, and decreased the binding of S2-013 cells to type I collagen, Type IV collagen and laminin. Similar effects were not observed for cells expressing tandem repeat-deleted MUC1 cDNA. Adhesion properties were abolished by benzyl-alpha-GalNAc treatment, indicating that glycosylation of the extracellular domain of MUC1 was essential for these biological adhesive functions. Our data support the hypothesis that MUC1 expression contributes to the metastatic ability of pancreatic cancer cells. 2000 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11058865&dopt=Abstract

Int J Cancer. 2000 Nov 15;88(4):593-600.
Extracellular lipid-mediated signaling in tumor-cell activation and pseudopod protrusion.

Hodgson L, Kohn EC, Dong C.

Department of Bioengineering, Pennsylvania State University, University Park, PA 16802, USA.

We have pioneered an in vitro pseudopod-generation model wherein suspended tumor cells are stimulated to form pseudopods into glass micropipettes in response to soluble collagen type IV (CIV). Pertussis toxin and removing intracellular calcium were found previously to be inhibitory to that process. We now extend those observations to dissect the roles of transmembrane calcium influx and circulating fatty acids on pseudopod extension. Removal of fatty acids from BSA in basal media resulted in abrogation of pseudopod formation, while reconstitution of free fatty acids restored cell pseudopod protrusion. We thus hypothesized that fatty acids may provide necessary pseudopod stimulatory signals. Addition of lysophosphatidic acid (LPA) to the fatty acid-free CIV solution or in an opposite pipette without CIV permitted approximately 50% pseudopod recovery in all pipette directions in a dose-dependent fashion. Thapsigargin (TG), an agent that releases internal calcium stores and causes opening of store-operated calcium channels, restored pseudopod protrusion up to 80% in CIV with fatty acid-free albumin. [Ca(2+)](i) release was non-additive when cells were stimulated by TG and LPA, suggesting overlapping [Ca(2+)](i) stores. The combination of TG and LPA in fatty acid-free albumin fully restored the pseudopod response to CIV. Addition of EGTA to chelate stimulatory media calcium blocked the pseudopod response to CIV in the presence of fatty acids. This indicates that pseudopod protrusion requires transmembrane calcium entry. Thus, extracellular lipids and calcium mobilization are required to complement CIV in pseudopod protrusion from suspended cells. 2000 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11058876&dopt=Abstract

Zhonghua Gan Zang Bing Za Zhi. 2000 Oct;8(5):274-5.
[Expression of collagen XVIII mRNA in rat liver fibrosis]

[Article in Chinese]

Jia J, Bauer M, Boigk G, Ruehl M, Schuppan D, Wang B.

Liver Research Center, Beijing Friendship Hospital, Capital University of Medical Sciences, Beijing 100050, China.

OBJECTIVE: To measure and study quantitatively the collagen XVIII mRNA in normal and fibrotic rat livers. METHODS: We used ribonuclease protection assay to investigate the collagen XVIII mRNA expression in rat liver fibrosis induced by complete bile duct occlusion (BDO). The expression level of procollagen 1 (XVIII) mRNA was compared with that of procollagen 1 (I) and tissue inhibitor of metalloproteinase 1 (TIMP1). RESULTS: mRNA levels of procollagen and TIMP 1 increased 20- and 4-fold in BDO rat livers, respectively. In contrast, hepatic procollagen 1 mRNA level increased only 1.8-fold in fibrotic rat livers. CONCLUSION: C XVIII mRNA is upregulated slightly in liver fibrosis, which is probably correlated with the fact that CXVIII is mainly expressed by hepatocytes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11058949&dopt=Abstract

Zhonghua Gan Zang Bing Za Zhi. 2000 Oct;8(5):279-81.
[Regulation of transcription factors c-myb and liver activator protein on expression of alpha1(I) collagen gene in activated hepatic stellate cells]

[Article in Chinese]

Liu X.

Department of Internal Medicine, First Affiliated Hospital of West China University of Medical Sciences, Chengdu 610041, China.

OBJECTIVE: To elucidate the role of two transcription factors, c-myb and liver activator protein (LAP, a member of the C/EBP family) in the expression of alpha1(I) collagen gene in activated hepatic stellate cells (HSCs). METHODS: Rat HSCs were prepared from SD rats by in situ perfusion and single-step density Nycodenz gradient. Two chimeric luciferase reporter gene plasmids containing the human collagen alpha1(I) gene promoter fragments (-804 approximately +1452 or -804 approximately +222) were constructed. Culture-activated HSCs were co-transfected with the reporter gene constructs and mammalian vectors expressing c-myb or/and LAP using the cationic-liposome mediated method. RESULTS: Transient transfection of the vector expressing LAP significantly increased basal transcription from PGL(3)-col and PGL(3)-col (intron) reporter gene vectors [(587 +/- 62)U/mg protein vs (315 +/- 45)U/mg protein and (326 +/- 52)U vs (220 +/- 70)U, t=10.4 and 3.6, respectively, both P<0.05]. C-myb showed no transactivation to both PGL(3)-col and PGL(3)-col (intron) reporter gene vectors. But co-expression of LAP and c-myb increased basal transcription from PGL(3)-col reporter gene by approximate 3 fold (1261 +/- 130)U vs (315 +/- 45)U, t=20.6, P<0.01. Moreover, co-expression of a specific c-myb antisense vector with the LAP vector inhibited the transactivation of LAP to collagen alpha1(I) gene promoter activity (334 +/- 29)U vs (315 +/- 45)U, t=1.06, P>0.05), which was observed only in PGL(3)-col plasmids. CONCLUSION: The transcription factor LAP transactivates collagen alpha1(I) gene in activated HSCs. C-myb plays an important role in transcriptional regulation of alpha1(I) collagen gene in HSCs and this effect is mediated by the transcription factor LAP and the cis-acting element in the first intron of alpha1(I) collagen gene.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11058951&dopt=Abstract

Zhonghua Gan Zang Bing Za Zhi. 2000 Oct;8(5):285-7.
Fas ligand expression and apoptosis in primary rat hepatocytes induced by lipopolysaccharide.

[Article in Chinese]

Yao Y, Zhang D, Luo Y, Zhang D, Huang A, Zhou W, Ren H.

Institute for Viral Hepatitis, Chongqing University of Medical Sciences, Chongqing 400010, China.

OBJECTIVE: To study hepatocyte apoptosis induced by lipopolysaccharide (LPS) directly and indirectly, and to elucidate the mechanisms of liver damage in endotoxemia. METHODS: Rat hepatocytes were isolated using collagenase perfusion, and cultured in RPMI 1640 medium. After 24h or 48 h of LPS treatment at various concentrations (1, 5, 10 mug/ml), membrane-bound Fas ligand (mFasL) expression in hepatocytes was determined by immunocytochemistry, and apoptosis was detected by TUNEL. In another set of experiments it was examined whether LPS-treated hepatocytes and its supernatants can stimulate apoptosis in LPS-untreated hepatocytes. RESULTS: LPS markedly stimulated mFasL expression and apoptosis in hepatocytes in a dose and time (24-48 h) dependent manner. In the co-culture system LPS-treated hepatocytes significantly induced LPS-untreated hepatocyte apoptosis. In contrast, there was no apoptotic cells observed in the supernatant stimulation system. CONCLUSION: LPS not only directly causes hepatocyte apoptosis, but also indirectly induces apoptosis of LPS-untreated hepatocytes by way of stimulating mFasL expression in hepatocytes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11058953&dopt=Abstract

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