Gentamicin, a read‐through agent for the treatment of rectal cancer

Frumkin, Jesse P.

doi:10.1111/codi.13832

Cited by 3 publications

(2 citation statements)

References 5 publications

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“…Interestingly, Lei et al (2017) demonstrated that quercetin, a flavonoid widely present in vegetables and fruits, potentiated the efficacy of anticancer drugs [27]. Recently, GM has been described as a read-through agent for the treatment of rectal cancer [28]. This is the first study showing the action of GM in human gastric cancer NCI-N87 cells.…”

Section: Discussionmentioning

confidence: 99%

Gentamicin Targets Acid Sphingomyelinase in Cancer: The Case of the Human Gastric Cancer NCI-N87 Cells

Albi

Cataldi

Ceccarini

et al. 2019

IJMS

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Emerging literature implicates acid sphingomyelinase in tumor sensitivity/resistance to anticancer treatments. Gentamicin is a drug commonly used as an antimicrobial but its serendipity effects have been shown. Even though many evidences on the role of gentamicin in cancer have been reported, its mechanism of action is poorly understood. Here, we explored acid sphingomyelinase as a possible new target of gentamicin in cancer. Since gastric cancer is one of the most common cancers and represents the second cause of death in the world, we performed the study in NCI-N87 gastric cancer cell line. The effect of the drug resulted in the inhibition of cell proliferation, including a reduction of cell number and viability, in the decrease of MIB-1 proliferative index as well as in the upregulation of cyclin-dependent kinase inhibitor 1A and 1B (CDKN1A and CDKN1B), and growth arrest and DNA-damage 45A (GADD45A) genes. The cytotoxicity was apoptotic as shown by FACS analysis. Additionally, gentamicin reduced HER2 protein, indicating a minor tumor aggressiveness. To further define the involvement of sphingomyelin metabolism in the response to the drug, gene and protein expression of acid and neutral sphingomeylinase was analyzed in comparison with phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and vitamin D receptor (VDR), molecules involved in cancer. Gentamicin induced a downregulation of PTEN, VDR, and neutral sphingomyelinase and a strong upregulation of acid sphingomyelinase. Of note, we identified the same upregulation of acid sphingomyelinase upon gentamicin treatment in other cancer cells and not in normal cells. These findings provide new insights into acid sphingomyelinase as therapeutic target, reinforcing studies on the potential role of gentamicin in anticancer therapy.

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Section: Discussionmentioning

confidence: 99%

Gentamicin Targets Acid Sphingomyelinase in Cancer: The Case of the Human Gastric Cancer NCI-N87 Cells

Albi

Cataldi

Ceccarini

et al. 2019

IJMS

View full text Add to dashboard Cite

show abstract

“…The paper by Frumkin 2017 contained an error. The Chi‐Square statistic mentioned in the following sentence is incorrect ‘Using Mathematica 11 (Wolfram Research, Inc., Champaign, Illinois, USA), we can apply the log‐rank test for censored interval data [5] to assess the tabulated data and reject the hypothesis that the hazard rates are equal ( P = 0.0223, X 2 = 0.023316; q = 0; γ = 0).’ The correct statistic should be X 2 = 7.6035 instead of 0.023316.…”

mentioning

confidence: 99%

Corrigendum

2018

Colorectal Disease

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CorrigendumThe paper by Frumkin 2017 [1] contained an error. The Chi-Square statistic mentioned in the following sentence is incorrect 'Using Mathematica 11 (Wolfram Research, Inc., Champaign, Illinois, USA), we can apply the log-rank test for censored interval data [5] to assess the tabulated data and reject the hypothesis that the hazard rates are equal (P = 0.0223, X 2 = 0.023316; q = 0; c = 0).' The correct statistic should be X 2 = 7.6035 instead of 0.023316.The exact value and significance of the P-value remains correct as published.

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Unraveling the Anti-Cancer Mechanisms of Antibiotics: Current Insights, Controversies, and Future Perspectives

Karamanolis,

Kounatidis,

Vallianou

et al. 2024

Antibiotics

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Cancer persists as a significant global health challenge, claiming millions of lives annually despite remarkable strides in therapeutic innovation. Challenges such as drug resistance, toxicity, and suboptimal efficacy underscore the need for novel treatment paradigms. In this context, the repurposing of antibiotics as anti-cancer agents has emerged as an attractive prospect for investigation. Diverse classes of antibiotics have exhibited promising anti-cancer properties in both in vitro and in vivo studies. These mechanisms include the induction of apoptosis and cell cycle arrest, generation of reactive oxygen species, and inhibition of key regulators of cell proliferation and migration. Additional effects involve the disruption of angiogenesis and modulation of pivotal processes such as inflammation, immune response, mitochondrial dynamics, ferroptosis, and autophagy. Furthermore, antibiotics have demonstrated the potential to enhance the efficacy of conventional modalities like chemotherapy and radiotherapy, while alleviating treatment-induced toxicities. Nevertheless, the integration of antibiotics into oncological applications remains contentious, with concerns centered on their disruption of gut microbiota, interference with immunotherapeutic strategies, contribution to microbial resistance, and potential association with tumorigenesis. This narrative review explores the mechanisms of antibiotics’ anti-cancer activity, addresses controversies about their dual role in cancer biology, and envisions future perspectives that include the development of novel derivatives and innovative frameworks for their incorporation into cancer treatment paradigms.

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Gentamicin, a read‐through agent for the treatment of rectal cancer

Cited by 3 publications

References 5 publications

Gentamicin Targets Acid Sphingomyelinase in Cancer: The Case of the Human Gastric Cancer NCI-N87 Cells

Gentamicin Targets Acid Sphingomyelinase in Cancer: The Case of the Human Gastric Cancer NCI-N87 Cells

Corrigendum

Unraveling the Anti-Cancer Mechanisms of Antibiotics: Current Insights, Controversies, and Future Perspectives

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