Profiling of differential expression of messenger RNA in normal, benign, and metastatic prostate cell lines

Chakrabarti, Ratna; Robles, Liza D.; Gibson, Jane; Muroski, Megan E.

doi:10.1016/s0165-4608(02)00641-6

Cited by 25 publications

(10 citation statements)

References 36 publications

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“…A marked difference in the composition of fatty acids and the gene expression profile between prostate cancer and BPH cells or tissues has been described. 29,30 This implies the disassociation of the Ser447stop polymorphism with risk of BPH, while the Ser447stop polymorphism is specifically involved in the development of prostate cancer by affecting fatty acid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Association of lipoprotein lipase gene polymorphism with risk of prostate cancer in a japanese population

Narita

Tsuchiya

Wang

et al. 2004

Intl Journal of Cancer

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Prostate cancer has a prominent variation in incidence among different racial/ethnic groups. Previous studies have demonstrated that nutritional factors, especially fat intake, may contribute to the development and progression of prostate cancer. In fact, animal studies have shown that lower fat intake inhibits prostate cancer growth. 1,2 Giovannucci et al. 3 have demonstrated a marked increase in the likelihood of prostate cancer in men with a high fat intake from red meat and a significant association between the total intake of essential fatty acids such as ␣-linolenic acid and the development of aggressive prostate cancer. On the other hand, the significance of genetic factors in the development and progression of prostate cancer has been well documented. While the incidence of prostate cancer in the native Japanese population is 5 times lower than that in Caucasians, Japanese Americans have an approximately 40 -50% higher rate of prostate cancer than Japanese men, but the rate of prostate cancer in Japanese American men does not appear to approach that of Caucasians. 4,5 These reports further support the concept that genetic factors in combination with dietary factors may have a significant impact on susceptibility to prostate cancer. In exploring genetic susceptibility factors for prostate cancer, a population whose nutritional or environmental factors are small may be an ideal cohort, in which individual differences in such factors and gene-environment interactions are minimized. It has been reported that the calorie intake and the proportion of fat to total calories consumed are quite low in Japan compared to those in Western countries. 6 Therefore, the Japanese might be an ideal population to investigate the association between polymorphisms and prostate cancer risk because the nutritional factors may be minimized.Lipoprotein lipase (LPL) plays a crucial role in fat metabolism. LPL hydrolyses triglycerides in both chylomicrons and very-lowdensity lipoproteins (VLDLs) and liberates free fatty acids. The human LPL gene is localized to chromosome 8p22. The gene contains 10 exons and has several DNA variants designated as Ser447stop, HindIII and PvuII polymorphisms. These polymorphisms have been shown to underlie changes in plasma lipoprotein levels and to be one of the important risk factors for cardiovascular diseases. 7-9 However, no information is available on the relationship between these LPL polymorphisms and prostate cancer risk.In this study, with the hypothesis that the LPL polymorphisms may be associated with the onset and/or progression of prostate cancer, we analyzed the LPL genotype of patients with prostate cancer or benign prostatic hyperplasia (BPH) as compared with male controls in a native Japanese population. MATERIAL AND METHODS SubjectsA total of 708 subjects consisting of 273 prostate cancer patients, 205 BPH patients and 230 male controls who visited Akita University Medical Center, its related community hospitals and Kyoto University Hospital were enrolled in this study. Because thi...

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Section: Discussionmentioning

confidence: 99%

Association of lipoprotein lipase gene polymorphism with risk of prostate cancer in a japanese population

Narita

Tsuchiya

Wang

et al. 2004

Intl Journal of Cancer

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“…To overcome this problem, it is critical to understand the mechanism in which prostate cancers will progress and metastasize. Metastatic prostate cancer proceeds through a series of distinct states, such as transformation of normal prostatic epithelial cell to preinvasive primary tumor, androgen-dependent invasive cancer, and androgen-independent metastatic disease (Chakrabarti et al, 2002). These stages of prostate cancer involve multiple molecular changes some of which can be implicated in metastatic process (Dong et al, 1995;Sheng et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Up-regulation of defense enzymes is responsible for low reactive oxygen species in malignant prostate cancer cells

Lim

Hong²,

Jin³

et al. 2005

Exp Mol Med

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“…Therefore, it is likely that Rac-mediated activation of actin reorganization is mediated through LIMK1. cDNA microarry and differential display reverse-transcription PCR analyses revealed an up-regulation of LIMK1 mRNA (25) and LIMK1 as the elastin-linked gene (26) in prostate adenocarcinoma cells. This study reports that LIMK1 is overexpressed in prostate adnocarcinomatous tissues and in malignant prostate cell lines and is essential for the invasive property and growth of prostate cancer cells, and the effect is not mediated through inactivating phosphorylation of cofilin.…”

mentioning

confidence: 99%

LIM Kinase 1 Is Essential for the Invasive Growth of Prostate Epithelial Cells

Dávila

Frost

Grizzle

et al. 2003

Journal of Biological Chemistry

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137

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Mammalian LIM kinase 1 (LIMK1) is involved in reorganization of actin cytoskeleton through inactivating phosphorylation of the ADF family protein cofilin, which depolymerizes actin filaments. Maintenance of the actin dynamics in an ordered fashion is essential for stabilization of cell shape or promotion of cell motility depending on the cell type. These are the two key phenomena that may become altered during acquisition of the metastatic phenotype by cancer cells. Here we show that LIMK1 is overexpressed in prostate tumors and in prostate cancer cell lines, that the concentration of phosphorylated cofilin is higher in metastatic prostate cancer cells, and that a partial reduction of LIMK1 altered cell proliferation by arresting cells at G 2 /M, changed cell shape, and abolished the invasiveness of metastatic prostate cancer cells. We also show that the ectopic expression of LIMK1 promotes acquisition of invasive phenotype by the benign prostate epithelial cells. Our data provide evidence of a novel role of LIMK1 in regulating cell division and invasive property of prostate cancer cells and indicate that the effect is not mediated by phosphorylation of cofilin. Our study correlates with the recent observations showing a metastasisassociated chromosomal gain on 7q11.2 in prostate cancer, suggesting a possible gain in LIMK1 DNA (7q11.23).LIM kinase 1 (LIMK1) 1 belongs to a novel dual specificity (serine/threonine and tyrosine) kinase family that contain two amino-terminal LIM domains (1). LIMK1 gene is expressed predominantly in brain and in developing neural tissues (2), and its deletion (microdeletion of chromosome 7q11.23) is typical for Williams syndrome (3). Cofilin, one of the actin-binding proteins, considered to be a potent regulator of the actin dynamics (4) by means of its activity in F-actin depolymerization, is the only known substrate of LIMK1. The function of cofilin is inhibited by phosphorylation at the Ser-3 residue (5) by LIMK1, which leads to accumulation of F-actin. The catalytic activity of LIMK1 is regulated by distinct members of the Rho subfamily of small GTPases (Rho, Rac, and Cdc42), which controls actin filament dynamics and focal adhesions assembly in response to extra-and intracellular stimuli. Rho, Rac, and Cdc42 induce formation of stress fibers, assembly of lamellipodia and membrane ruffles, and regulation of filopodial protrusions, respectively (6). LIMK1 has been shown to mediate specifically Rac-induced actin cytoskeleton reorganization and focal adhesion complexes (5, 7, 8). Rac-induced activation of LIMK1 is mediated by PAK1, which phosphorylates LIMK1 on its Thr 508 residue (9). Other studies also proposed that Rhoand Cdc42-induced cytoskeletal changes are mediated through phosphorylation of LIMK1 by Rho-dependent protein kinase ROCK (10) and Cdc42-regulated protein kinase PAK4 (11) and MRCK␣ (12).The non-catalytic domain of LIMK1 contains two tandem repeats of a LIM motif, a putative zinc binding motif, and a PDZ domain, which contains two tandem nuclear exit signal sequence...

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Profiling of differential expression of messenger RNA in normal, benign, and metastatic prostate cell lines

Cited by 25 publications

References 36 publications

Association of lipoprotein lipase gene polymorphism with risk of prostate cancer in a japanese population

Association of lipoprotein lipase gene polymorphism with risk of prostate cancer in a japanese population

Up-regulation of defense enzymes is responsible for low reactive oxygen species in malignant prostate cancer cells

LIM Kinase 1 Is Essential for the Invasive Growth of Prostate Epithelial Cells

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