Sodium salicylate inhibits proliferation and induces G1 cell cycle arrest in human pancreatic cancer cell lines

Perugini, Richard A.; McDade, Theodore P.; Vittimberga, Frank J.; Duffy, Andrew; Callery, Mark P.

doi:10.1016/s1091-255x(00)80029-3

Cited by 56 publications

(31 citation statements)

References 29 publications

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“…Caspase-3 activation, an early indicator of apoptosis, was evident within 12 h of mitogen stimulation. Our proliferation assays involved a model of serum starvation to induce cell quiescence [Perugini et al, 2000]. Both MTT and BrDU assays showed that 26S proteasome inhibition blocked proliferation vs. FCS alone.…”

Section: Discussionmentioning

confidence: 99%

26S proteasome inhibition induces apoptosis and limits growth of human pancreatic cancer

Shah

Potter

McDade

et al. 2001

J of Cellular Biochemistry

244

138

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The 26S proteasome degrades proteins that regulate transcription factor activation, cell cycle progression, and apoptosis. In cancer, this may allow for uncontrolled cell division, promoting tumor growth, and spread. We examined whether selective inhibition of the 26S proteasome with PS-341, a dipeptide boronic acid analogue, would block proliferation and induce apoptosis in human pancreatic cancer. Proteasome inhibition significantly blocked mitogen (FCS) induced proliferation of BxPC3 human pancreatic cancer cells in vitro, while arresting cell cycle progression and inducing apoptosis by 24 h. Accumulation of p21(Cip1-Waf-1), a cyclin dependent kinase (CDK) inhibitor normally degraded by the 26S proteasome, occurred by 3 h and correlated with cell cycle arrest. When BxPC3 pancreatic cancer xenografts were established in athymic nu/nu mice, weekly administration of 1 mg/kg PS-341 significantly inhibited tumor growth. Both cellular apoptosis and p21(Cip1-Waf-1) protein levels were increased in PS-341 treated xenografts. Inhibition of tumor xenograft growth was greatest (89%) when PS-341 was combined with the tumoricidal agent CPT-11. Combined CPT-11/PS-341 therapy, but not single agent therapy, yielded highly apoptotic tumors, significantly inhibited tumor cell proliferation, and blocked NF-kappaB activation indicating this systemic therapy was effective at the cancer cell level. 26S proteasome inhibition may represent a new therapeutic approach against this highly resistant and lethal malignancy.

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Section: Discussionmentioning

confidence: 99%

26S proteasome inhibition induces apoptosis and limits growth of human pancreatic cancer

Shah

Potter

McDade

et al. 2001

J of Cellular Biochemistry

244

138

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“…It was reported that NASAIDs can arrest HT-29 cell cycle at the G 0 /G 1 phase by inhibiting the expression of cdc2, cdc4 and cyclin, decreasing the phosphorylation of Rb, and increasing the p21 WAF-1/CIPL expression in HT-29 cells [17] . Moreover, Perugini [18] found that aspirin induces cell cycle arrest at the G 1 phase in human pancreatic cancer cells by inhibiting cyclinD1. Whether aspirin shares the same mechanism against SW480 cells still needs to be explored.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms underlying aspirin-mediated growth inhibition and apoptosis induction of cyclooxygenase-2 negative colon cancer cell line SW480

Lai¹,

Huang²,

Liang³

et al. 2008

WJG

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AIM:To investigate the effects of aspirin (acetylsalicylic acid) on proliferation and apoptosis of colorectal cancer cell line SW480 and its mechanism. METHODS: Cyclooxygenase (COX)-2 negative colorectal cancer cell line SW480 was treated with aspirin at concentrations of 2.5 mmol/L, 5.0 mmol/L, 10.0 mmol/L for different periods in vitro . Anti-proliferation effect of aspirin on SW480 was detected by 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle and apoptosis were observed by flow cytometry (FCM). Transmission electron microscope (TEM) was used for morphological study. Apoptosis-associated genes were detected by immunohistochemical staining and Western blotting.

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“…A second group of researchers assessed the effect of salicylate on human pancreatic carcinoma cell lines. 51 Cells treated with salicylate demonstrated significantly inhibited cell proliferation, and less progression from the G 1 phase to the S-phase.…”

Section: Animal and Ex Vivo Studiesmentioning

confidence: 93%

Chemoprevention of gastrointestinal malignancies with nonsteroidal antiinflammatory drugs

Shaheen

Straus

Sandler

2002

Cancer

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In multiple studies, the chronic use of nonsteroidal antiinflammatory drugs (NSAIDs) has been associated with a decreased incidence of several types of gastrointestinal (GI) neoplasia. This effect may be mediated by one of several intracellular mechanisms, some of which involve the inhibition of the cyclooxygenase-2 (COX-2) isoenzyme. In multiple studies of colorectal carcinoma, chronic NSAID use has shown a protective effect, with the majority of studies demonstrat-

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Sodium salicylate inhibits proliferation and induces G1 cell cycle arrest in human pancreatic cancer cell lines

Cited by 56 publications

References 29 publications

26S proteasome inhibition induces apoptosis and limits growth of human pancreatic cancer

26S proteasome inhibition induces apoptosis and limits growth of human pancreatic cancer

Mechanisms underlying aspirin-mediated growth inhibition and apoptosis induction of cyclooxygenase-2 negative colon cancer cell line SW480

Chemoprevention of gastrointestinal malignancies with nonsteroidal antiinflammatory drugs

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