Alteration of tumor growth by aspirin and indomethacin: Studies with two transplantable tumors in mouse

Hial, Valdemar; Horakova, Zdenka; Shaff, Richard E.; Beaven, Michael A.

doi:10.1016/0014-2999(76)90044-3

Cited by 145 publications

(35 citation statements)

References 18 publications

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“…* indicates P50.05 compared to the mock-irradiated group transfected with pRL-TK+3' UTR PGE 2 have been described in basal cell carcinomas with an aggressive growth pattern (Vanderveen et al, 1986). Inhibitors of prostaglandin production and their ability to inhibit tumor growth and metastasis provide evidence for the role of prostaglandins in tumorigenesis (Buckman et al, 1998;Hial et al, 1976;Lynch et al, 1978;Snyderman et al, 1995). These studies demonstrate the possible role that COX-2 plays in the promotion of skin tumors and illustrate the need for inhibitors of COX-2.…”

Section: Discussionmentioning

confidence: 73%

The role of p38 in UVA-induced cyclooxygenase-2 expression in the human keratinocyte cell line, HaCaT

2002

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Section: Discussionmentioning

confidence: 73%

The role of p38 in UVA-induced cyclooxygenase-2 expression in the human keratinocyte cell line, HaCaT

2002

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“…This hypothesis is not supported by the observation that cyclooxygenase inhibitors like indomethacin are unable to influence the growth of tumour cells in vivo (Feldman and Hilf, 1985;Abou-El-Ela et al, 1989). In addition, the effects of indomethacin on various in vitro models show that it can either stimulate or inhibit tumour cell proliferation (Buckman et al, 1991;Fulton, 1984;Rose and Connolly, 1990;Bayer et al, 1979;Hial et al, 1977). Other studies have suggested that increased lipid peroxidation may be an important cause of cytotoxicity associated with n-3 PUFAs but a definite role has not been established (Falconer et al, 1994;Lystad et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Cell cycle arrest and induction of apoptosis in pancreatic cancer cells exposed to eicosapentaenoic acid in vitro

Lai

Ross²,

Fearon³

et al. 1996

Br J Cancer

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Summary Eicosapentaenoic acid (EPA) has been shown to have an inhibitory effect on the growth of several pancreatic cancer cell lines in vitro. This study investigates the mechanism of growth inhibition and cytotoxicity of EPA on the pancreatic cancer cell line MIA PaCa-2. Cells were analysed for cell count, viability, cell cycle distribution and ultrastructural changes. There was a time-and dose-dependent decrease in cell count and viability in cultures of pancreatic cancer cells supplemented with EPA. Flow cytometric DNA anlaysis of MIA PaCa-2 cells incubated with EPA demonstrated the presence of sub G1 populations corresponding to the presence of apoptotic cells and the blockade of cell cycle progression in S-phase and G2/M-phase. The presence of apoptosis in EPA-supplemented cultures was further confirmed by DNA fragmentation and ultrastructural changes associated with apoptosis. Therefore, we conclude that EPA mediates its effect on the pancreatic cancer cell line MIA PaCa-2, at least in part, via cell cycle arrest and the induction of apoptosis.

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“…COX-2 regulation of proliferation (Sheng et al, 1997;Nguyen and Lee, 1993;Hial et al, 1977), apoptosis (Tsujii and DuBois, 1995;Watson, 1998;Wolf and Laster, 1999), and tumor-blood vessel interaction (Tsujii et al, 1998) has been suggested. Recent evidence implicates the prostaglandin receptor, peroxisome proliferator-activated receptor delta (PPAR-d), as a mediator in prostaglandin regulated tumorigenesis (He et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Cyclooxygenase-two (COX-2) modulates proliferation in aggressive fibromatosis (desmoid tumor)

Poon

Smits

et al. 2001

Oncogene

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Aggressive ®bromatosis is a locally invasive soft tissue lesion. Seventy-®ve per cent of cases harbor a somatic mutation in either the APC or b-catenin genes, resulting in b-catenin protein stabilization. Cyclooxygenase-2 (COX-2) is an enzyme involved in prostaglandin synthesis that modulates the formation of colonic neoplasia, especially in cases due to mutations resulting in b-catenin stabilization. Human aggressive ®broma-toses and lesions from the Apc+/Apc1638N mouse (a murine model for Apc-driven ®bromatosis) demonstrated elevated COX-2 levels. COX-2 blockade either by the selective agent DFU or by non-selective COX blocking agents results in reduced proliferation in human tumor cell cultures. Breeding mice with Cox-27/7 mice resulted in no di erence in number of aggressive ®bromatoses formed, but in a smaller tumor size, while there was a decrease in number of GI lesions by 50%. Mice fed various COX blocking agents also showed a decline in tumor size. COX-2 expression was regulated by tcf-dependent transcription in this lesion. COX-2 partially regulates proliferation due to b-catenin stabilization in aggressive ®bromatosis. Although COX blockade alone does not cause tumor regression, this data suggests that it may have a role as an adjuvant therapy to slow tumor growth in this lesion. Oncogene (2001) 20, 451 ± 460.

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Alteration of tumor growth by aspirin and indomethacin: Studies with two transplantable tumors in mouse

Cited by 145 publications

References 18 publications

The role of p38 in UVA-induced cyclooxygenase-2 expression in the human keratinocyte cell line, HaCaT

The role of p38 in UVA-induced cyclooxygenase-2 expression in the human keratinocyte cell line, HaCaT

Cell cycle arrest and induction of apoptosis in pancreatic cancer cells exposed to eicosapentaenoic acid in vitro

Cyclooxygenase-two (COX-2) modulates proliferation in aggressive fibromatosis (desmoid tumor)

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