Aspirin inhibits the proliferation and migration of gastric cancer cells in p53-knockout mice

Li, Xue-Fu; Xu, Bing-Zhong; Wang, Shizhen

doi:10.3892/ol.2016.5067

Cited by 7 publications

(5 citation statements)

References 20 publications

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“…Therefore, the present study investigated these stemness-related proteins to determine the relationship between p53 and stemness. Similar to previous studies (41,46,47), the expression levels of stemness-related proteins, such as lin28B, Sox2, c-Myc, Sall4 and oct4 were increased in p53 +/and p53 -/-mBM-MScs, suggesting a positive role of p53 inactivation in stemness maintenance.…”

Section: Discussionsupporting

confidence: 87%

“…Previous studies in primary murine cells reported that p53 accumulation and stabilization could promote increased apoptosis and induce cell cycle arrest (46,47). The present study demonstrated, through growth curve assays and dna cell cycle analysis, that p53 +/and p53 -/-mBM-MScs possessed a higher proliferative potential compared with p53 +/+ mBM-MScs, and that the absence, or partial absence, of p53 corresponded with an increased S phase rate within the cell cycle compared with basal p53 levels.…”

Section: Discussionmentioning

confidence: 99%

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Mouse bone marrow mesenchymal stem cells with distinct p53 statuses display differential characteristics

Wang

Mao

et al. 2020

Mol Med Report

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Mesenchymal stem cells (MScs) affect diverse aspects of tumor progression, such as angiogenesis, tumor growth and metastasis. Bone marrow MScs (BM-MScs) are fibroblast-like cells with multipotent differentiation ability, that localize to areas of tissue damage, including wounds and solid tumors. The tumor suppressor gene, p53, is functionally involved in cell cycle control, apoptosis and genomic stability, and is mutated and inactivated in most human cancers. The present study aimed to investigate the role of p53 in the biology of BM-MScs. in the present study, p53 wild-type (p53 +/+), knockdown (p53 +/-) and knockout (p53-/-) mouse BM-MScs (mBM-MSCs) were observed to be similar in appearance and in the expression of cell surface biomarkers, but expressed differential p53 protein levels. The p53 +/and p53-/-mBM-MScs demonstrated an increased proliferation rate compared with mBM-MScs derived from p53 +/+ mice. mBM-MScs from all three groups, representing distinct p53 statuses, were unable to form tumors over a 3-month period in vivo. The adipogenic and osteogenic differentiation of mBM-MScs was increased in the absence of p53. The colony formation and migratory abilities of p53 +/and p53-/-mBM-MSCs were markedly enhanced, and the expression levels of stem cell-associated proteins were significantly increased compared with p53 +/+. The expression levels of microrna (mir)-3152 and mir-337 were significantly increased in p53 +/and p53-/-mBM-MScs, whereas the expression levels of mir-221, mir-155, mir-1288 and miR-4669 were significantly decreased. The expression levels of tumor necrosis factor-α and interferon-γ-inducible protein-10 were significantly upregulated in the supernatant of p53 +/and p53-/-mBM-MSCs. Ubiquitin protein ligase E3 component n-recognin 2, RING-finger protein 31 and matrix metalloproteinase 19 were highly expressed in p53 +/and p53-/-mBM-MScs. The results of the present study indicated that p53 may serve an important role in the biology of mBM-MSCs, and may provide novel insights into the role of cells with different p53 statuses in cancer progression.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Mouse bone marrow mesenchymal stem cells with distinct p53 statuses display differential characteristics

Wang

Mao

et al. 2020

Mol Med Report

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“…It's well known that aspirin depresses cell proliferation in many cancers [29][30][31][32][33][34]. To test the effects of aspirin on liver cancer cells, we performed cell viability, colony-formation and EdU assays in HepG2 and H7402 cells with different concentrations of aspirin.…”

Section: Aspirin Inhibits the Proliferation Of Liver Cancer Cells In mentioning

confidence: 99%

Aspirin inhibits the proliferation of hepatoma cells through controlling GLUT1-mediated glucose metabolism

et al. 2018

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Aspirin can efficiently inhibit liver cancer growth, but the mechanism is poorly understood. In this study, we report that aspirin modulates glucose uptake through downregulating glucose transporter 1 (GLUT1), leading to the inhibition of hepatoma cell proliferation. Our data showed that aspirin significantly decreased the levels of reactive oxygen species (ROS) and glucose consumption in hepatoma cells. Interestingly, we identified that GLUT1 and HIF1α could be decreased by aspirin. Mechanically, we demonstrated that the -1008/-780 region was the regulatory element of transcriptional factor NF-κB in GLUT1 promoter by luciferase report gene assays. PDTC, an inhibitor of NF-κB, could suppress the expression of GLUT1 in HepG2 and H7402 cells, followed by affecting the levels of ROS and glucose consumption. CoCl-activated HIF1α expression could slightly rescue the GLUT1 expression inhibited by aspirin or PDTC, suggesting that aspirin depressed GLUT1 through targeting NF-κB or NF-κB/HIF1α signaling. Moreover, we found that GLUT1 was highly expressed in clinical HCC tissues relating to their paired adjacent normal tissues. Importantly, we observed that high level of GLUT1 was significantly correlated with the poor relapse-free survival of HCC patients by analysis of public data. Functionally, overexpression of GLUT1 blocked the PDTC-induced or aspirin-induced inhibition of glucose metabolism in HepG2 cells. Conversely, aspirin failed to work when GLUT1 was stably knocked down in the cells. Administration of aspirin could depress the growth of hepatoma cells through controlling GLUT1 in vitro and in vivo. Thus, our finding provides new insights into the mechanism by which aspirin depresses liver cancer.

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Section: Prosmentioning

confidence: 99%

“…A previous study using animal experiments suggested that aspirin may inhibit not only the growth of gastric cancer but also the migration of cancer cells ( 36 ). Li et al ( 36 ) used p53 − / − mice (n=20) that were randomly divided into 2 groups to understand the effects of aspirin on gastric cancer. The aforementioned study demonstrated that the proliferation capacity of tumor cells in the experimental group (250 mg/kg aspirin daily added to food) was significantly reduced compared with that of the control group, and the number of cells was also markedly reduced.…”

Section: Prosmentioning

confidence: 99%

Effects of aspirin on the gastrointestinal tract: Pros vs. cons (Review)

Wang

Shen

et al. 2020

Oncol Lett

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Acetylsalicylic acid, also known as aspirin, is often used in clinical antipyretic, analgesic and antiplatelet therapy. Aspirin can cause numerous side effects in the gastrointestinal (GI) tract, ranging from unpleasant GI symptoms without gastric mucosal lesions to ulcer bleeding and even death. However, recent studies have found that aspirin can significantly prevent GI tumors. Despite impressive advances in cancer research, screening and treatment options, GI tumors remain a leading cause of death worldwide. Prevention is a far better option than treatment for tumors. Therefore, the present review assesses the pros and cons of aspirin on the GI tract and, on this the basis, the appropriate dose of aspirin to protect it. Contents

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Aspirin inhibits the proliferation and migration of gastric cancer cells in p53-knockout mice

Cited by 7 publications

References 20 publications

Mouse bone marrow mesenchymal stem cells with distinct p53 statuses display differential characteristics

Mouse bone marrow mesenchymal stem cells with distinct p53 statuses display differential characteristics

Aspirin inhibits the proliferation of hepatoma cells through controlling GLUT1-mediated glucose metabolism

Effects of aspirin on the gastrointestinal tract: Pros vs. cons (Review)

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