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Reynolds, Sharon; Cederberg, Hokan; Chakrabarty, Subhas

doi:10.1023/a:1011071907047

Cited by 14 publications

(6 citation statements)

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“…Ectopic expression of the PAF receptor in normal rat kidney mesenchymal fibroblasts, however, has been reported to suppress v-src-or v-ras-induced transformation (Kume and Shimizu, 1997). We had earlier shown that 1-O(2-methoxy) hexadecyl glycerol, a lipid with similar aliphatic fatty acid chains to that of PAF is biologically active and suppresses the malignant properties of human colon and prostate cancer cells (Wang et al, 1999;Reynolds et al, 2000). In this study, we showed that PAF-activated MAP kinases, induced a more differentiated phenotype and suppressed the malignant properties of human colon carcinoma cells.…”

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confidence: 53%

“…(Figure 1b). Since the induction of Waf1/p21 is associated with growth inhibition and the induction of differentiation (Di Cunto et al, 1998;Chakrabarty et al, 1998), we determined the effect of PAF on CEA production, a differentiationrelated marker for colon carcinomas (Chakrabarty et al, 1988;Guadagni et al, 1990;Reynolds et al, 1998Reynolds et al, , 2000Wang et al, 1999). A one-time treatment of these cells (healthy and actively proliferating) with PAF (5-10 mm) induced a significant increase in CEA production Figure 2 Effect of PAF on anchorage-independent growth and cellular invasion.…”

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confidence: 99%

“…Since the induction of differentiation of colon carcinoma cells is associated with a suppression of their malignant phenotype (Reynolds et al, 1998(Reynolds et al, , 2000Wang et al, 1999), we determined the effect of PAF on the malignant properties of these cells. Malignant properties were assessed in terms of the propensity to grow in soft agarose or anchorage-independent growth, and to invade a matrigel matrix or cellular invasion (Reynolds et al, 1998(Reynolds et al, , 2000Wang et al, 1999). These experiments were performed using healthy viable cells in medium containing serum because serum starvation itself would suppress growth in agarose (a 10-day culture period) and cellular invasion (a 4-day culture period).…”

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Platelet-activating factor activates mitogen-activated protein kinases, inhibits proliferation, induces differentiation and suppresses the malignant phenotype of human colon carcinoma cells

Wang

Chakrabarty

2003

Oncogene

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Recent studies suggest that the action of plateletactivating factor (PAF), a potent phospholipid modulator of allergic and inflammatory reactions, is diverse and functions as a modulator of a variety of physiological and pathological events in many cell types and tissues. Its role (if any) in modulating the proliferation, transformation and/or differentiation of epithelial colonic cells, however, is not known. In this study, we showed that PAF is biologically active in epithelial-derived human colon carcinoma cells with different phenotypic properties. These cells expressed the PAF receptor. PAF activated three prominent mitogen-activated protein kinase modules (ERK, p38MAPK and Jun N-terminal kinases) in these cells, inhibited proliferation and induced differentiation (measured by the induction of Waf1/p21 and the induction of the differentiation-related marker CEA). The net effect of PAF treatment was the suppression of malignant cell behavior (measured by anchorage-independent growth and cellular invasion). It is concluded that PAF is a modulator of proliferation and differentiation in human epithelialderived colon carcinoma cells.

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confidence: 53%

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Platelet-activating factor activates mitogen-activated protein kinases, inhibits proliferation, induces differentiation and suppresses the malignant phenotype of human colon carcinoma cells

Wang

Chakrabarty

2003

Oncogene

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“…Both human prostate cancer LnCap and DU145 cell lines have responded to the antiproliferative effect of MHG in a similar manner [48]. …”

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confidence: 99%

“…[48] observed that both the human prostate cancer LnCap and DU145 cell lines responded to the antiproliferative effect of MHG in a similar manner. In this study MHG inhibited cell growth with equal potency in these cell lines with an IC-50 value of 93 μM for LnCap, and 97 μM for DU145 while the IC-50 values for phenylbutyrate were 1.3 mM and 7.3 mM, respectively, for LnCap and DU145 cells.…”

Section: Alkylglycerols Studiesmentioning

confidence: 99%

An Update on the Therapeutic Role of Alkylglycerols

Iannitti

Palmieri

2010

Marine Drugs

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Scandinavian folk medicine used shark liver oil for the treatment of cancers and other ailments based on the rarity of tumors in sharks and their ability to resist infections. Shark liver oil is a source of alkylglycerols which have been studied as anti-cancer agents in several clinical trials. Moreover, alkylglycerols have been investigated for the treatment of radiation induced side effects and for their ability to boost the immune system. Several experimental studies have shown the ability of alkylglycerols to open the blood brain barrier to facilitate the access of therapeutic drugs to the central nervous system. This review covers the most important studies of alkylglycerols in both animals and humans.

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Phenylbutyrate inhibits the invasive properties of prostate and breast cancer cell lines in the sea urchin embryo basement membrane invasion assay

Dyer

Paulsen

Markwart

et al. 2002

Intl Journal of Cancer

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Histone deacetylase inhibitors, such as phenylbutyrate, are currently undergoing clinical trials as potential anticancer agents. Phenylbutyrate can induce cell differentiation and apoptosis in a number of cancer cell types and can act in synergy with ionizing radiation and chemotherapy to induce apoptosis. We used the sea urchin embryo basement membrane invasion assay to show that phenylbutyrate potently inhibited the invasive properties of both prostate and breast cancer cells at clinically achievable doses. This inhibition was dose-dependent and persisted for at least 24 hr after the drug was removed. These results suggest that in addition to activating apoptosis in cancer cells, phenylbutyrate may be used in prevention of metastatic disease. 4 -7 It has been shown that butyrate and phenylbutyrate can act in synergy with radiation 8 -11 or chemotherapy 11,12 to induce cells to undergo apoptosis. Furthermore, some HDAC inhibitors have recently been found to inhibit angiogenesis. 13 The anti-angiogenic properties of HDAC inhibitors may occur through the down regulation of VEGF expression. 10 In our previous study we found that phenylbutyrate reduced the expression of caveolin-1. 10 Although the exact role of caveolin-1 in carcinogenesis is unclear, caveolin-1 is thought to regulate integrin signaling 14 and high expression of caveolin-1 is associated with a metastatic phenotype in breast and prostate cancer. [15][16][17] In addition to reducing caveolin-1 expression, phenylbutyrate has been found to reduce the expression of the invasion-related plasminogen activator, urokinase, in glioma cells 18 and reduce the invasiveness of cancer cells in artificial matrigel chamber invasion assays. 18,19 We explored the ability of phenylbutyrate to block the invasiveness of metastatic prostate and breast cancer cells using the sea urchin embryo basement membrane invasion assay. This invasion assay utilizes the natural occurring, selectively permeable basement membranes of sea urchin embryos (SU-ECM) as invasion substrates. 20,21 The sea urchin embryo basement membrane is functionally analogous to the mammalian basement membranes underlying the epidermis because it is invaded by pigment cells during development. 22 We have shown previously that these SU-ECM invasion substrates can be selectively invaded by metastatic tumor cells. 20 In fact, we have shown that this assay can predict the metastatic potential of cancer cell lines with greater than 99% confidence. 20 We show that phenylbutyrate effectively inhibits the invasiveness of metastatic prostate and breast cancer cells in the SU-ECM invasion assay. MATERIAL AND METHODS Cell cultures and phenylbutyrate treatmentsPC3 and DU-145 cells were obtained from American Type Culture Collection (Manassas, VA) and Steve Ethier, University of Michigan, kindly provided us with the SUM-149 cell line. The PC3 and DU-145 cells were cultured in MEM (Life Technologies, Grand Island, NY) supplemented with 10% FBS (HyClone, Logan, UT), with 1ϫ amino acids, vitamins and antibiotics. SUM-1...

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Cited by 14 publications

References 36 publications

Platelet-activating factor activates mitogen-activated protein kinases, inhibits proliferation, induces differentiation and suppresses the malignant phenotype of human colon carcinoma cells

Platelet-activating factor activates mitogen-activated protein kinases, inhibits proliferation, induces differentiation and suppresses the malignant phenotype of human colon carcinoma cells

An Update on the Therapeutic Role of Alkylglycerols

Phenylbutyrate inhibits the invasive properties of prostate and breast cancer cell lines in the sea urchin embryo basement membrane invasion assay

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