Aspirin and cancer: biological mechanisms and clinical outcomes

Elwood, Peter Creighton; Protty, Majd; Morgan, Gareth; Pickering, Janet Elizabeth; Delon, Christine; Watkins, John

doi:10.1098/rsob.220124

Cited by 32 publications

(15 citation statements)

References 88 publications

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“…Aspirin is involved in the proliferation and apoptosis of cancer cells through cyclooxygenase inhibition 29 . Furthermore, several signaling pathways are regulated in the antitumor process of aspirin.…”

Section: Discussionmentioning

confidence: 99%

“…Aspirin is involved in the proliferation and apoptosis of cancer cells through cyclooxygenase inhibition. 29 Furthermore, several signaling pathways are regulated in the antitumor process of aspirin. The PI3K/AKT/mTOR pathway is a classic signaling pathway that regulates cell survival, proliferation, metabolism, and growth, which is a promising target for antitumor agents including aspirin.…”

Section: Discussionmentioning

confidence: 99%

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Aspirin boosts the synergistic effect of EGFR/p53 inhibitors on lung cancer cells by regulating AKT/mTOR and p53 pathways

Liu,

Cui,

Wang

et al. 2023

Cell Biochemistry & Function

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The regimen of afatinib and vinorelbine has been used to treat breast or lung cancer cells with some limitations. Aspirin alone or in combination with other agents has shown unique efficacy in the treatment of cancer. We designed a preclinical study to investigate whether the triple therapy of aspirin, afatinib, and vinorelbine could synergistically inhibit the growth of p53 wild‐type nonsmall cell lung cancer (NSCLC) cells. Three NSCLC cells A549, H460, and H1975 were selected to study the effect of triple therapy on cell proliferation and apoptosis. Compared to single agents, triple therapy synergistically inhibited the proliferation of lung cancer cells with combination index <1. Meanwhile, the therapeutic index of triple therapy was superior to that of single agents, indicating a balance between efficacy and safety in the combination of three agents. Mechanistic studies showed that triple therapy significantly induced apoptosis by decreasing mitochondrial membrane potential, increasing reactive oxygen species, and regulating mitochondria‐related proteins. Moreover, epidermal growth factor receptor (EGFR) downstream signaling proteins including JNK, AKT, and mTOR were dramatically suppressed and p53 was substantially increased after NSCLC cells were exposed to the triple therapy. We provided evidence that the triple therapy of aspirin, afatinib and vinorelbine synergistically inhibited lung cancer cell growth through inactivation of the EGFR/AKT/mTOR pathway and accumulation of p53, providing a new treatment strategy for patients with p53 wild‐type NSCLC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Aspirin boosts the synergistic effect of EGFR/p53 inhibitors on lung cancer cells by regulating AKT/mTOR and p53 pathways

Liu,

Cui,

Wang

et al. 2023

Cell Biochemistry & Function

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“…Cyclooxygenase-2 (COX-2) is frequently expressed in various tumors and plays a role not only in promoting tumor development but also elevating the resistance to chemotherapy and radiotherapy [ 111 ]. Aspirin exerts its anticancer effects via inhibition of COX, interference with proliferative pathways, cancer-related inflammation, and antiplatelet-driven pro-carcinogenic activity [ 112 ]. However, there is a risk of gastrointestinal and intracranial hemorrhage and other adverse effects associated with the long-term application of large amounts of aspirin.…”

Section: Novel Synthetic H 2 S Releasing Drugmentioning

confidence: 99%

The potential role of hydrogen sulfide in cancer cell apoptosis

Gao,

Liu,

Zhang

et al. 2024

Cell Death Discov.

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For a long time, hydrogen sulfide (H2S) has been considered a toxic compound, but recent studies have found that H2S is the third gaseous signaling molecule which plays a vital role in physiological and pathological conditions. Currently, a large number of studies have shown that H2S mediates apoptosis through multiple signaling pathways to participate in cancer occurrence and development, for example, PI3K/Akt/mTOR and MAPK signaling pathways. Therefore, the regulation of the production and metabolism of H2S to mediate the apoptotic process of cancer cells may improve the effectiveness of cancer treatment. In this review, the role and mechanism of H2S in cancer cell apoptosis in mammals are summarized.

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“…To use anti-inflammatory drug aspirin or statin to repair ME degeneration-related tumor capsule disruptions. Previous studies have consistently demonstrated that aspirin or statin could significantly alter the chronic inflammation milieu of a variety of human cancers and prevent cancer progression 172 - 176 . Thus, the administration of aspirin or statin to individuals with focally disrupted MECL associated with significant infiltration of immune cells (as shown in Figure 10 ) may potentially reduce the extent of infiltrating immune cells.…”

Section: Specific Applications Of Mecl In Detection and Interventions...mentioning

confidence: 99%

The most likely but largely ignored triggering factor for breast (or all) cancer invasion

Man¹,

Mannion²,

Stojadinovic³

et al. 2023

J. Cancer

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Breast cancer development and progression are believed to be a sequential process, from normal to hyperplastic, to in situ , and to invasive and metastatic stages. Given that over 90% of cancer deaths are caused by invasive and metastatic lesions, countless factors and multiple theories have been proposed as the triggering factor for the cascade of actions of cancer invasion. However, those factors and theories are largely based on the studies of cell lines or animal models. In addition, corresponding interventions based on these factors and theories have failed to reduce the incidence rate of invasive and metastatic lesions, suggesting that previous efforts may have failed to arm at the right target. Considering these facts and observations, we are proposing “A focal aberrant degeneration in the myoepithelial cell layer (MECL) as the most likely triggering factor for breast cancer invasion”. Our hypothesis is based on our recent studies of breast and multiple other cancers. Our commentary provides the rationale, morphologic, immunohistochemical, and molecular data to support our hypotheses. As all epithelium-derived cancers share a very similar architecture, our hypothesis is likely to be applicable to invasion of all cancer types. We believe that human tissue-derived data may provide a more realistic roadmap to guide the clinic practice.

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Aspirin and cancer: biological mechanisms and clinical outcomes

Cited by 32 publications

References 88 publications

Aspirin boosts the synergistic effect of EGFR/p53 inhibitors on lung cancer cells by regulating AKT/mTOR and p53 pathways

Aspirin boosts the synergistic effect of EGFR/p53 inhibitors on lung cancer cells by regulating AKT/mTOR and p53 pathways

The potential role of hydrogen sulfide in cancer cell apoptosis

The most likely but largely ignored triggering factor for breast (or all) cancer invasion

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