Therapeutic potential of Fingolimod in triple negative breast cancer preclinical models

Rupp, Tristan; Pelouin, Océane; Genest, Laurie; Legrand, Christophe; Froget, Guillaume; Castagné, Vincent

doi:10.1016/j.tranon.2020.100926

Cited by 20 publications

(32 citation statements)

References 79 publications

(83 reference statements)

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“…Previous studies also showed that administrating cisplatin to mice significantly reduced their body weight [20][21][22]. A lower body weight in the cisplatin treatment group than in control group is also observed in breast cancer-bearing mice [23]. Accordingly in our study, the body weight was lower in the cisplatin treatment group than in the control group.…”

Section: Discussionsupporting

confidence: 75%

Fatty Acid Binding Protein 6 Inhibition Decreases Cell Cycle Progression, Migration and Autophagy in Bladder Cancers

Lin

Chang

Lai

et al. 2022

IJMS

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Bladder cancer (BC) has a high recurrence rate worldwide. The aim of this study was to evaluate the role of fatty acid binding protein 6 (FABP6) in proliferation and migration in human bladder cancer cells. Cell growth was confirmed by MTT and colony formation assay. Western blotting was used to explore protein expressions. Wound healing and Transwell assays were performed to evaluate the migration ability. A xenograft animal model with subcutaneous implantation of BC cells was generated to confirm the tumor progression. Knockdown of FABP6 reduced cell growth in low-grade TSGH-8301 and high-grade T24 cells. Cell cycle blockade was observed with the decrease of CDK2, CDK4, and Ki67 levels in FABP6-knockdown BC cells. Interestingly, knockdown of FBAP6 led to downregulation of autophagic markers and activation of AKT-mTOR signaling. The application of PI3K/AKT inhibitor decreased cell viability mediated by FABP6-knockdown additionally. Moreover, FABP6-knockdown reduced peroxisome proliferator-activated receptor γ and retinoid X receptor α levels but increased p-p65 expression. Knockdown of FABP6 also inhibited BC cell motility with focal adhesive complex reduction. Finally, shFABP6 combined with cisplatin suppressed tumor growth in vivo. These results provide evidence that FABP6 may be a potential target in BC cells progression.

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Section: Discussionsupporting

confidence: 75%

Fatty Acid Binding Protein 6 Inhibition Decreases Cell Cycle Progression, Migration and Autophagy in Bladder Cancers

Lin

Chang

Lai

et al. 2022

IJMS

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“…Epidemiological studies on DMTs show data disparity 4 , although second-line immunosuppressants (azathioprine, cyclophosphamide, mitoxantrone) seem to involve a heightened risk for malignancy 22 . However, the relationship between immunotherapy and neoplasm development is inconclusive since some of these drugs are employed as coadjuvants or even anti-cancer drugs (ALB, cladribine, mitoxantrone) ( http://www.ema.europa.eu ), or are under consideration (FLM, TER) as oncologic therapeutic options 7 , 23 . This implies their subjection by Medicines Agencies to the monitoring of the possible development of malignancy in treated MS patients.…”

Section: Discussionmentioning

confidence: 99%

Potential risk of disease modifying therapies on neoplasm development and coadjutant factors in multiple sclerosis outpatients

Gil-Bernal

González-Caballero

Espinosa-Rosso

et al. 2021

Sci Rep

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Neoplasm development in Multiple Sclerosis (MS) patients treated with disease-modifying therapies (DMTs) has been widely discussed. The aim of this work is to determine neoplasm frequency, relationship with the prescription pattern of DMTs, and influence of the patients’ baseline characteristics. Data from 250 MS outpatients were collected during the period 1981–2019 from the medical records of the Neurology Service of the HUPM (Hospital Universitario Puerta del Mar)—in Southern Spain—and analysed using Cox models. Neoplasm prevalence was 24%, mainly located on the skin, with cancer prevalence as expected for MS (6.8%). Latency period from MS onset to neoplasm diagnosis was 10.4 ± 6.9 years (median 9.30 [0.9–30.5]). During the observation period β-IFN (70.4% of patients), glatiramer acetate (30.4%), natalizumab (16.8%), fingolimod (24.8%), dimethyl fumarate (24.0%), alemtuzumab (6.0%), and teriflunomide (4.8%) were administered as monotherapy. Change of pattern in step therapy was significantly different in cancer patients vs unaffected individuals (p = 0.011) (29.4% did not receive DMTs [p = 0.000]). Extended Cox model: Smoking (HR = 3.938, CI 95% 1.392–11.140, p = 0.010), being female (HR = 2.006, 1.070–3.760, p = 0.030), and age at MS diagnosis (AGE-DG) (HR = 1.036, 1.012–1.061, p = 0.004) were risk factors for neoplasm development. Secondary progressive MS (SPMS) phenotype (HR = 0.179, 0.042–0.764, p = 0.020) and treatment-time with IFN (HR = 0.923, 0.873–0.977, p = 0.006) or DMF (HR = 0.725, 0.507–1.036, p = 0.077) were protective factors. Tobacco and IFN lost their negative/positive influence as survival time increased. Cox PH model: Tobacco/AGE-DG interaction was a risk factor for cancer (HR = 1.099, 1.001–1.208, p = 0.049), followed by FLM treatment-time (HR = 1.219, 0.979–1.517). In conclusion, smoking, female sex, and AGE-DG were risk factors, and SPMS and IFN treatment-time were protective factors for neoplasm development; smoking/AGE-DG interaction was the main cancer risk factor.

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“…Using immunomodulating or immunosuppressive drugs is unfortunately accompanied by high risk of cancer development due to involvement of immune system in recognizing and eliminating cancer cells [182]. On the other hand, some available MS DMTs have been used for years in cancer therapy (e.g., rituximab [184], cladribine [185] and methotrexate [186]), while other current DMTs are being evaluated in the present for their anti-tumor potential (e.g., dimethylfumarate [187], fingolimod [188] and teriflunomide [189]).…”

Section: Cannabinoids and Multiple Sclerosismentioning

confidence: 99%

Endocannabinoid Modulation in Neurodegenerative Diseases: In Pursuit of Certainty

Vasincu

Rusu

Ababei

et al. 2022

Biology

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Neurodegenerative diseases are an increasing cause of global morbidity and mortality. They occur in the central nervous system (CNS) and lead to functional and mental impairment due to loss of neurons. Recent evidence highlights the link between neurodegenerative and inflammatory diseases of the CNS. These are typically associated with several neurological disorders. These diseases have fundamental differences regarding their underlying physiology and clinical manifestations, although there are aspects that overlap. The endocannabinoid system (ECS) is comprised of receptors (type-1 (CB1R) and type-2 (CB2R) cannabinoid-receptors, as well as transient receptor potential vanilloid 1 (TRPV1)), endogenous ligands and enzymes that synthesize and degrade endocannabinoids (ECBs). Recent studies revealed the involvement of the ECS in different pathological aspects of these neurodegenerative disorders. The present review will explore the roles of cannabinoid receptors (CBRs) and pharmacological agents that modulate CBRs or ECS activity with reference to Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Huntington’s Disease (HD) and multiple sclerosis (MS).

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Therapeutic potential of Fingolimod in triple negative breast cancer preclinical models

Cited by 20 publications

References 79 publications

Fatty Acid Binding Protein 6 Inhibition Decreases Cell Cycle Progression, Migration and Autophagy in Bladder Cancers

Fatty Acid Binding Protein 6 Inhibition Decreases Cell Cycle Progression, Migration and Autophagy in Bladder Cancers

Potential risk of disease modifying therapies on neoplasm development and coadjutant factors in multiple sclerosis outpatients

Endocannabinoid Modulation in Neurodegenerative Diseases: In Pursuit of Certainty

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