Aspirin use reduces skin-cancer risk

McCaffrey, Pat

doi:10.1016/s1470-2045(05)70523-4

Cited by 4 publications

(3 citation statements)

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“…Aspirin, also known as acetylsalicylic acid, is a non-steroidal anti-inflammatory drug, which is non-toxic to humans ( 19 ). Previous clinical and epidemiological studies have demonstrated that long-term treatment with aspirin may decrease the risk of colorectal, breast, prostate, lung and skin cancer ( 8 , 10 , 12 ). However, whether aspirin may promote cellular apoptosis and inhibit proliferation and invasion remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Aspirin, which is one of the most common therapeutic drugs worldwide, was primarily introduced as an anti-inflammatory and analgesic agent ( 7 ). Nevertheless, clinical and epidemiological studies have demonstrated that aspirin may decrease the risk of several types of cancer, including colorectal, breast, prostate, lung and skin cancer ( 8 – 12 ). The anticancer effects of aspirin may be dependent on its ability to induce apoptosis or inhibit proliferation in cancer cells.…”

Section: Introductionmentioning

confidence: 99%

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Effects of aspirin on proliferation, invasion and apoptosis of Hep‑2 cells via the PTEN/AKT/NF‑κB/survivin signaling pathway

Jin

Zhang³

et al. 2018

Oncol Lett

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Aspirin may exhibit antitumor activities, as it is able to inhibit cell proliferation. However, the ability of aspirin to inhibit cellular proliferation in Hep-2 cells and its underlying molecular mechanisms have been poorly determined. The aim of the present study was to investigate whether aspirin may induce cell apoptosis in the neoplastic cell line Hep-2. The effects of aspirin on the migratory and invasive abilities of Hep-2 cells were also investigated using Transwell assays. In the present study, it was demonstrated that aspirin induced apoptosis and inhibited proliferation, migration and invasion in Hep-2 cells. Aspirin also significantly decreased the expression of B-cell lymphoma 2 (Bcl-2) and caspase-3, and increased the expression of Bcl-2-associated X protein, suggesting that aspirin induced apoptosis through the intrinsic apoptotic pathway. Hep-2 cells treated with aspirin exhibited a significant upregulation of phosphatase and tensin homolog (PTEN) and decreased levels of phosphorylated protein kinase B (AKT). However, the total amount of AKT protein was not altered in response to aspirin treatment. Furthermore, the expression of nuclear factor (NF)-κB and survivin, which are the downstream targets of the PTEN/AKT signaling pathway, was inhibited. These results indicated that the molecular mechanism underlying the antitumor effects of aspirin may be associated with the inhibition of tumor invasion and induction of apoptosis by regulating the activity of the PTEN/AKT/NF-κB/survivin signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of aspirin on proliferation, invasion and apoptosis of Hep‑2 cells via the PTEN/AKT/NF‑κB/survivin signaling pathway

Jin

Zhang³

et al. 2018

Oncol Lett

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“…2 In addition to its classical anti-inflammatory function, clinical and epidemiological studies have also demonstrated that prolonged aspirin use reduces the risk of colorectal, breast, prostate, lung and skin cancers. 3, 4, 5, 6, 7 The anticancer effect of aspirin is attributable to its ability to induce apoptosis or inhibit cell proliferation. The mechanism of aspirin's therapeutic effects has been established as the irreversible inhibition of cyclooxygenases (COXs) by cross-acetylation.…”

Section: Introductionmentioning

confidence: 99%

Aspirin-induced Bcl-2 translocation and its phosphorylation in the nucleus trigger apoptosis in breast cancer cells

et al. 2013

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Here, we report that B-cell lymphoma 2 (Bcl-2) is a novel target molecule of aspirin in breast cancer cells. Aspirin influenced the formation of a complex by Bcl-2 and FKBP38 and induced the nuclear translocation of Bcl-2 and its phosphorylation. These events inhibited cancer cell proliferation and subsequently enhanced MCF-7 breast cancer cell apoptosis. Bcl-2 knockdown using small interfering RNA (siRNA) delayed apoptotic cell death, which correlated with increased proliferation following aspirin exposure. In contrast, Bcl-2 overexpression enhanced the onset of aspirin-induced apoptosis, which was also associated with a significant increase in Bcl-2 phosphorylation in the nucleus. Therefore, this study may provide novel insight into the molecular mechanism of aspirin, particularly its anticancer effects in Bcl-2- and estrogen receptor-positive breast cancer cells.

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No Chemopreventive Effect of Nonsteroidal Anti-Inflammatory Drugs on Nonmelanoma Skin Cancer: Evidence from Meta-Analysis

Zhang

Liang

Ye³

et al. 2014

PLoS ONE

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BackgroundNonmelanoma skin cancer (NMSC),which includes squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), is the most common form of cancer, and its incidence is increasing. Nonsteroidal anti-inflammatory drugs (NSAIDs) have been reported to be chemopreventive for NMSC. However, the results from published studies were controversial.MethodsWe searched the PubMed and Embase databases for relevant studies. Moreover, relevant reviews regarding the use of NSAIDs for NMSC patients were examined for potential inclusive studies. To measure the effects of NSAIDs, the relative risk (RR) was analyzed.ResultsA Total of 8 studies were included in our meta-analysis. We found that NSAIDs use was not associated with a reduced risk of SCC or BCC under the random effects model (pooled RR = 0.86, 95% CI, 0.73–1.02, P = 0.085; pooled RR = 0.94, 95% CI 0.85–1.04, P = 0.266; respectively).ConclusionFrom the included studies, we found no statistically significant chemopreventive effect on NMSC of NSAIDs. This finding warrants more prospective studies evaluating the relationship between NSAIDs and NMSC.

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Aspirin use reduces skin-cancer risk

Cited by 4 publications

References 0 publications

Effects of aspirin on proliferation, invasion and apoptosis of Hep‑2 cells via the PTEN/AKT/NF‑κB/survivin signaling pathway

Effects of aspirin on proliferation, invasion and apoptosis of Hep‑2 cells via the PTEN/AKT/NF‑κB/survivin signaling pathway

Aspirin-induced Bcl-2 translocation and its phosphorylation in the nucleus trigger apoptosis in breast cancer cells

No Chemopreventive Effect of Nonsteroidal Anti-Inflammatory Drugs on Nonmelanoma Skin Cancer: Evidence from Meta-Analysis

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