Proliferation inhibition of cisplatin‐resistant ovarian cancer cells using drugs screened by integrating a metabolic model and transcriptomic data

Motamedian, Ehsan; Taheri, Elham; Bagheri, Fatemeh

doi:10.1111/cpr.12370

Cited by 10 publications

(11 citation statements)

References 39 publications

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“…To our knowledge, this is the first study that combines proteomics data with this type of computational analyses to study drug’s mechanism of actions in breast cancer. However, FBA was successfully used in ovarian cancer cells to propose new therapeutic targets and to study the effect of drugs targeting metabolism and their synergies [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Molecular characterization of breast cancer cell response to metabolic drugs

et al. 2018

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Metabolic reprogramming is a hallmark of cancer. It has been described that breast cancer subtypes present metabolism differences and this fact enables the possibility of using metabolic inhibitors as targeted drugs in specific scenarios. In this study, breast cancer cell lines were treated with metformin and rapamycin, showing a heterogeneous response to treatment and leading to cell cycle disruption. The genetic causes and molecular effects of this differential response were characterized by means of SNP genotyping and mass spectrometry-based proteomics. Protein expression was analyzed using probabilistic graphical models, showing that treatments elicit various responses in some biological processes such as transcription. Moreover, flux balance analysis using protein expression values showed that predicted growth rates were comparable with cell viability measurements and suggesting an increase in reactive oxygen species response enzymes due to metformin treatment. In addition, a method to assess flux differences in whole pathways was proposed. Our results show that these diverse approaches provide complementary information and allow us to suggest hypotheses about the response to drugs that target metabolism and their mechanisms of action.

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Section: Discussionmentioning

confidence: 99%

Molecular characterization of breast cancer cell response to metabolic drugs

et al. 2018

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“…During the past decade, various algorithms for integration of omics data and metabolic models have been developed to predict the anti‐tumor effect of non‐oncological drugs . The algorithm of transcriptional regulated flux balance analysis aimed to construct cancer cell‐specific models has successfully identified terbinafine as a potential anti‐tumor drug . Existing evidence suggests that terbinafine suppresses the proliferation of colon cancer cell line by the involvement of the p53‐associated signaling pathway .…”

Section: Discussionmentioning

confidence: 99%

“…Recent evidence suggests that terbinafine, which is commonly used for the treatment of superficial mycosis, might have an anti‐tumor effect. An in silico analysis by integrating a generic human metabolic model with transcriptomic data found that terbinafine can inhibit the proliferation of resistant cancer cells while minimally affecting normal cells . Experimental data has shown that terbinafine can decrease the proliferation in various cultured human malignant cells with a dose‐dependent effect .…”

Section: Introductionmentioning

confidence: 99%

“…An in silico analysis by integrating a generic human metabolic model with transcriptomic data found that terbinafine can inhibit the proliferation of resistant cancer cells while minimally affecting normal cells. 14 Experimental data has shown that terbinafine can decrease the proliferation in various cultured human malignant cells with a dose-dependent effect. 15 Furthermore, mouse model studies have suggested that terbinafine might play a crucial role in the regulation of cancer progression and tumor angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Use of terbinafine and risk of death in patients with prostate cancer: A population‐based cohort study

Sundquist

2018

Intl Journal of Cancer

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Terbinafine is used for the treatment of several superficial fungal infections. In silico analyses and animal models suggest that terbinafine might have an anti‐tumor effect. We aimed to explore whether subsequent administration of terbinafine might be associated with a lower mortality rate in patients with prostate cancer. We identified patients diagnosed with prostate cancer between July 2005 and December 2014 from the Swedish Cancer Registry, and linked them to the Swedish Prescribed Drug Register to ascertain subsequent use of terbinafine. A total of 799 patients received oral treatment of terbinafine during the study period with a mortality rate of 18.6 per 1,000 person‐years. Compared to patients who did not use terbinafine and adjusting for a range of confounding factors, patients that received oral treatment of terbinafine had a decreased risk of death from prostate cancer (HR, 0.53; 95% CI, 0.38–0.73) and a decreased risk of death overall (HR, 0.64; 95% CI, 0.52–0.77). To account for indication bias, we further identified 907 patients who received topical use of terbinafine. However, the risk of death from prostate cancer in patients with topical use of terbinafine was 0.92 (95% CI 0.74–1.12) and the risk of death overall was 1.03 (95% CI 0.91–1.17) as compared to the controls, which suggests that there was no association between risk of death in patients with prostate cancer with topical use of terbinafine. These findings suggest that this drug's potential anti‐tumor effect needs to be explored further.

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“…Besides, there is still a lack of mature and convincing theory on specific and precise cellular molecular mechanisms of the initiation and development of HCC. 5 Decrypting the underlying molecular mechanisms of cell biology will shed light on the complex molecular and cellular pathways that mediate the initiation and progression of HCC. In addition, it will provide a potential treatment strategy against HCC.…”

Section: Introductionmentioning

confidence: 99%

SLC6A8 Knockdown Suppresses the Invasion and Migration of Human Hepatocellular Carcinoma Huh-7 and Hep3B Cells

Yuan

et al. 2020

Technol Cancer Res Treat

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Liver cancer is considered the sixth most commonly diagnosed cancer and the fourth leading cause of cancer-related deaths worldwide. Currently, there is no specific and effective therapy for hepatocellular carcinoma. Therefore, developing novel diagnostic and therapeutic strategies against hepatocellular carcinoma is of paramount importance. Solute carrier family 6 member 8 (SLC6A8) encodes the solute carrier family 6-8 to transport creatine into cells in a Na+ and Cl-- dependent manner. SLC6A8 deficiency is characterized by intellectual disabilities, loss of speech, and behavioral abnormalities. Of concern, the association of SLC6A8 with hepatocellular carcinoma remains elusive. In this study, we revealed that SLC6A8 knockdown significantly induced apoptosis and suppressed the migration and invasion of Hep3B and Huh-7 cells. These findings depicted the vital role of SLC6A8 in the initiation and progression of human hepatocellular carcinoma.

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Proliferation inhibition of cisplatin‐resistant ovarian cancer cells using drugs screened by integrating a metabolic model and transcriptomic data

Abstract: The proposed strategy was successful to identify drugs effective on the viability of resistant cancer cells. This strategy can enhance the potency of treatments for drug-resistant cancer cells and provides the possibility of using existing drugs.

Cited by 10 publications

References 39 publications

Molecular characterization of breast cancer cell response to metabolic drugs

Molecular characterization of breast cancer cell response to metabolic drugs

Use of terbinafine and risk of death in patients with prostate cancer: A population‐based cohort study

SLC6A8 Knockdown Suppresses the Invasion and Migration of Human Hepatocellular Carcinoma Huh-7 and Hep3B Cells

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