Prostaglandin E2 production and metabolism in human breast cancer cells and breast fibroblasts. Regulation by inflammatory mediators

Schrey, M.P.; Patel, Kirti

doi:10.1038/bjc.1995.523

Cited by 139 publications

(70 citation statements)

References 42 publications

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“…Indeed, stimulation of c-fos and Egr-1 expression by arachidonic acid in 3T3 fibroblasts has been found to depend upon PGE2 formation (Danesch et al, 1994). However, at present, we do not know the exact nature of the supporting role of PGE2 in the homeostasis of prostate cancer cells, such as that recently described for breast cancer cells (Schrey and Patel, 1995). These investigators have found that breast fibroblasts, particularly under the influence of inflammatory mediators, such as interleukin l1 and bradykinin, provide a potentially rich source for PGE2 production in breast cancer cells, whereas significant contributions from the epithelial tumour component may be restricted to breast cancer cells exhibiting an invasive phenotype (Schrey and Patel, 1995).…”

Section: Discussionmentioning

confidence: 92%

Induction of cyclo-oxygenase-2 mRNA by prostaglandin E2 in human prostatic carcinoma cells

Dahiya²,

1997

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Summary Prostaglandins are synthesized from arachidonic acid by the enzyme cyclo-oxygenase. There are two isoforms of cyclooxygenases: COX-1 (a constitutive form) and COX-2 (an inducible form). COX-2 has recently been categorized as an immediate-early gene and is associated with cellular growth and differentiation. The purpose of this study was to investigate the effects of exogenous dimethylprostaglandin E2 (dmPGE2) on prostate cancer cell growth. Results of these experiments demonstrate that administration of dmPGE2 to growing PC-3 cells significantly increased cellular proliferation (as measured by the cell number), total DNA content and endogenous PGE2 concentration. DmPGE2 also increased the steady-state mRNA levels of its own inducible synthesizing enzyme, COX-2, as well as cellular growth to levels similar to those seen with fetal calf serum and phorbol ester. The same results were observed in other human cancer cell types, such as the androgen-dependent LNCaP cells, breast cancer MDA-MB-134 cells and human colorectal carcinoma DiFi cells. In PC-3 cells, the dmPGE2 regulation of the COX-2 mRNA levels was both time dependent, with maximum stimulation seen 2 h after addition, and dose dependent on dmPGE2 concentration, with maximum stimulation seen at 5 [sg ml-'. The non-steroidal anti-inflammatory drug flurbiprofen (5 FM), in the presence of exogenous dmPGE2, inhibited the up-regulation of COX-2 mRNA and PC-3 cell growth. Taken together, these data suggest that PGE2 has a specific role in the maintenance of human cancer cell growth and that the activation of COX-2 expression depends primarily upon newly synthesized PGE2, perhaps resulting from changes in local cellular PGE2 concentrations.

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Section: Discussionmentioning

confidence: 92%

Induction of cyclo-oxygenase-2 mRNA by prostaglandin E2 in human prostatic carcinoma cells

Dahiya²,

1997

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“…Because established cancer cell lines are poor indicators of the tumor biology, the pathophysiological relevance of this finding is unclear at present. However, previous studies have documented that COX-2 is overexpressed in some breast cancer tissues and that enhanced prostanoid synthesis is associated with mammary tumors (23)(24)(25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

“…Furthermore, enhanced synthesis of PGE 2 , a major product of COX-2, was observed in human breast cancer as well as in experimental murine mammary tumor tissues (24,25). It also has been shown that highly metastatic and estrogen-independent tumors secrete high levels of PGE 2 (24,26). Recently Liu and Rose (27) showed that a highly invasive, metastatic, and estrogen receptor-negative human breast cancer cell line, MDA-MB-231, expressed high levels of COX-2 in a constitutive manner, whereas non-metastatic, less invasive, and estrogen receptor positive MCF-7 human breast cancer cells expressed low levels of COX-2.…”

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confidence: 99%

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Serum Withdrawal-induced Post-transcriptional Stabilization of Cyclooxygenase-2 mRNA in MDA-MB-231 Mammary Carcinoma Cells Requires the Activity of the p38 Stress-activated Protein Kinase

Jang

Sánchez

Schaefers

et al. 2000

Journal of Biological Chemistry

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Overexpression of the cyclooxygenase-2 (COX-2) gene is observed in several neoplastic diseases. However, molecular mechanisms involved in the regulation of expression of COX-2 are not well understood. In this report, we describe a unique post-transcriptional regulatory mechanism of COX-2 mRNA stabilization in MDA-MB-231 cells, a highly metastatic cell line derived from a human mammary tumor. High levels of COX-2 mRNA, protein, and enzyme activity were induced by serum withdrawal, which were potently inhibited by the addition of serum or >100-kDa serum factor. Nuclear run-on analysis and actinomycin D chase experiments indicate that regulation is primarily at the level of post-transcriptional mRNA stability. Interestingly, SB203580, an inhibitor of the p38 stress-activated protein kinase (SAPK), and overexpression of the dominant-negative p38␣ construct potently inhibited the serum withdrawal-induced COX-2 mRNA levels. Indeed, the half-life of COX-2 mRNA decreased from 9 to 4.5 h after SB203580 treatment, suggesting that signal transduction by the p38 SAPK pathway is required for COX-2 mRNA stability.

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“…COX-2 expression is induced by cytokines and growth factors at sites of inflammation and is usually not detected in normal tissues [94]. Increased COX-2 expression and PGE 2 production has been reported in human colon carcinoma [95], breast cancer [96,97], renal cell carcinoma [98], and lung carcinoma [99].…”

Section: Pgementioning

confidence: 99%

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Sionov

Fridlender

Granot

2014

Cancer Microenvironment

336

261

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Neutrophils are myeloid cells that constitute 50-70 % of all white blood cells in the human circulation. Traditionally, neutrophils are viewed as the first line of defense against infections and as a major component of the inflammatory process. In addition, accumulating evidence suggest that neutrophils may also play a key role in multiple aspects of cancer biology. The possible involvement of neutrophils in cancer prevention and promotion was already suggested more than half a century ago, however, despite being the major component of the immune system, their contribution has often been overshadowed by other immune components such as lymphocytes and macrophages. Neutrophils seem to have conflicting functions in cancer and can be classified into anti-tumor (N1) and pro-tumor (N2) sub-populations. The aim of this review is to discuss the varying nature of neutrophil function in the cancer microenvironment with a specific emphasis on the mechanisms that regulate neutrophil mobilization, recruitment and activation.

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Prostaglandin E2 production and metabolism in human breast cancer cells and breast fibroblasts. Regulation by inflammatory mediators

Cited by 139 publications

References 42 publications

Induction of cyclo-oxygenase-2 mRNA by prostaglandin E2 in human prostatic carcinoma cells

Induction of cyclo-oxygenase-2 mRNA by prostaglandin E2 in human prostatic carcinoma cells

Serum Withdrawal-induced Post-transcriptional Stabilization of Cyclooxygenase-2 mRNA in MDA-MB-231 Mammary Carcinoma Cells Requires the Activity of the p38 Stress-activated Protein Kinase

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

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