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1. Kanaan GN, Ichim B, Gharibeh L, Maharsy W, Patten DA, Xuan JY, Reunov A, Marshall P, Veinot J, Menzies K, Nemer M, Harper ME: Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies. Redox Biol; 2018 Apr;14:509-521

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies.
  • Glutaredoxin 2 (GRX2), a mitochondrial glutathione-dependent oxidoreductase, is central to glutathione homeostasis and mitochondrial redox, which is crucial in highly metabolic tissues like the heart.
  • Previous research showed that absence of Grx2, leads to impaired mitochondrial complex I function, hypertension and cardiac hypertrophy in mice but the impact on mitochondrial structure and function in intact cardiomyocytes and in humans has not been explored.
  • We hypothesized that Grx2 controls cardiac mitochondrial dynamics and function in cellular and mouse models, and that low expression is associated with human cardiac dysfunction.
  • Here we show that Grx2 absence impairs mitochondrial fusion, ultrastructure and energetics in primary cardiomyocytes and cardiac tissue.
  • Moreover, provision of the glutathione precursor, N-acetylcysteine (NAC) to Grx2-/- mice did not restore glutathione redox or prevent impairments.
  • Using genetic and histopathological data from the human Genotype-Tissue Expression consortium we demonstrate that low GRX2 is associated with fibrosis, hypertrophy, and infarct in the left ventricle.
  • Altogether, GRX2 is important in the control of cardiac mitochondrial structure and function, and protects against human cardiac pathologies.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
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  • (PMID = 29101900.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Cardiac hypertrophy / Cardiac metabolism / Human heart / Mitochondria / Oxidative stress / Redox
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2. Angelova PR, Barilani M, Lovejoy C, Dossena M, Viganò M, Seresini A, Piga D, Gandhi S, Pezzoli G, Abramov AY, Lazzari L: Mitochondrial dysfunction in Parkinsonian mesenchymal stem cells impairs differentiation. Redox Biol; 2018 Apr;14:474-484
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mitochondrial dysfunction in Parkinsonian mesenchymal stem cells impairs differentiation.
  • Sporadic cases account for 90-95% of all patients with Parkinson's Disease (PD).
  • Atypical Parkinsonism comprises approximately 20% of all patients with parkinsonism.
  • Progressive Supranuclear Palsy (PSP) belongs to the atypical parkinsonian diseases and is histopathologically classified as a tauopathy.
  • Here, we report that mesenchymal stem cells (MSCs) derived from the bone marrow of patients with PSP exhibit mitochondrial dysfunction in the form of decreased membrane potential and inhibited NADH-dependent respiration.
  • Furthermore, mitochondrial dysfunction in PSP-MSCs led to a significant increase in mitochondrial ROS generation and oxidative stress, which resulted in decrease of major cellular antioxidant GSH.
  • Additionally, higher basal rate of mitochondrial degradation and lower levels of biogenesis were found in PSP-MSCs, together leading to a reduction in mitochondrial mass.
  • This phenotype was biologically relevant to MSC stemness properties, as it heavily impaired their differentiation into adipocytes, which mostly rely on mitochondrial metabolism for their bioenergetic demand.
  • The defect in adipogenic differentiation was detected as a significant impairment of intracellular lipid droplet formation in PSP-MSCs.
  • This result was corroborated at the transcriptional level by a significant reduction of PPARγ and FABP4 expression, two key genes involved in the adipogenic molecular network.
  • Our findings in PSP-MSCs provide new insights into the etiology of 'idiopathic' parkinsonism, and confirm that mitochondrial dysfunction is important to the development of parkinsonism, independent of the type of the cell.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
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  • (PMID = 29096320.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Mesenchymal stem cells / Parkinsonism / Progressive supranuclear palsy
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3. Frandsen JR, Narayanasamy P: Neuroprotection through flavonoid: Enhancement of the glyoxalase pathway. Redox Biol; 2018 Apr;14:465-473

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroprotection through flavonoid: Enhancement of the glyoxalase pathway.
  • The glyoxalase pathway functions to detoxify reactive dicarbonyl compounds, most importantly methylglyoxal.
  • The glyoxalase pathway is an antioxidant defense mechanism that is essential for neuroprotection.
  • Excessive concentrations of methylglyoxal have deleterious effects on cells, leading to increased levels of inflammation and oxidative stress.
  • Neurodegenerative diseases - including Alzheimer's, Parkinson's, Aging and Autism Spectrum Disorder - are often induced or exacerbated by accumulation of methylglyoxal.
  • Antioxidant compounds possess several distinct mechanisms that enhance the glyoxalase pathway and function as neuroprotectants.
  • Flavonoids are well-researched secondary plant metabolites that appear to be effective in reducing levels of oxidative stress and inflammation in neural cells.
  • Novel flavonoids could be designed, synthesized and tested to protect against neurodegenerative diseases through regulating the glyoxalase pathway.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
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  • (PMID = 29080525.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Antioxidant / Detoxification / Flavonoid / Glyoxalase pathway / Neurodegenerative disease / Neuron / Neurons viable / Neuroprotection
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4. Nazıroğlu M, Blum W, Jósvay K, Çiğ B, Henzi T, Oláh Z, Vizler C, Schwaller B, Pecze L: Menthol evokes Ca<sup>2+</sup> signals and induces oxidative stress independently of the presence of TRPM8 (menthol) receptor in cancer cells. Redox Biol; 2018 Apr;14:439-449
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Menthol evokes Ca<sup>2+</sup> signals and induces oxidative stress independently of the presence of TRPM8 (menthol) receptor in cancer cells.
  • Menthol is a naturally occurring monoterpene alcohol possessing remarkable biological properties including antipruritic, analgesic, antiseptic, anti-inflammatory and cooling effects.
  • Here, we examined the menthol-evoked Ca<sup>2+</sup> signals in breast and prostate cancer cell lines.
  • The effect of menthol (50-500µM) was predicted to be mediated by the transient receptor potential ion channel melastatin subtype 8 (TRPM8).
  • However, the intensity of menthol-evoked Ca<sup>2+</sup> signals did not correlate with the expression levels of TRPM8 in breast and prostate cancer cells indicating a TRPM8-independent signaling pathway.
  • Menthol-evoked Ca<sup>2+</sup> signals were analyzed in detail in Du 145 prostate cancer cells, as well as in CRISPR/Cas9 TRPM8-knockout Du 145 cells.
  • Menthol (500µM) induced Ca<sup>2+</sup> oscillations in both cell lines, thus independent of TRPM8, which were however dependent on the production of inositol trisphosphate.
  • Results based on pharmacological tools point to an involvement of the purinergic pathway in menthol-evoked Ca<sup>2+</sup> responses.
  • Finally, menthol (50-500µM) decreased cell viability and induced oxidative stress independently of the presence of TRPM8 channels, despite that temperature-evoked TRPM8-mediated inward currents were significantly decreased in TRPM8-knockout Du 145 cells compared to wild type Du 145 cells.

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  • (PMID = 29078169.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Ca(2+) oscillations / Menthol / Oxidative stress / Purinergic signaling / TRPM8
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5. Ibáñez-Cabellos JS, Pérez-Machado G, Seco-Cervera M, Berenguer-Pascual E, García-Giménez JL, Pallardó FV: Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening. Redox Biol; 2018 Apr;14:398-408
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening.
  • Loss of function of dyskerin (DKC1), NOP10 and TIN2 are responsible for different inheritance patterns of Dyskeratosis congenita (DC; ORPHA1775).
  • They are key components of telomerase (DKC1 and NOP10) and shelterin (TIN2), and play an important role in telomere homeostasis.
  • They participate in several fundamental cellular processes by contributing to Dyskeratosis congenita through mechanisms that are not fully understood.
  • Presence of oxidative stress was postulated to result from telomerase ablation.
  • However, the resulting disturbed redox status can promote telomere attrition by generating a vicious circle, which promotes cellular senescence.
  • This fact prompted us to study if acute loss of DKC1, NOP10 and TINF2 can promote redox disequilibrium as an early event when telomere shortening has not yet taken place.
  • We generated siRNA-mediated (DKC1, NOP10 and TINF2) cell lines by RNA interference, which was confirmed by mRNA and protein expression analyses.
  • No telomere shortening occurred in any silenced cell line.
  • Depletion of H/ACA ribonucleoproteins DKC1 and NOP10 diminished telomerase activity via TERC down-regulation, and produced alterations in pseudouridylation and ribosomal biogenesis.
  • An increase in the GSSG/GSH ratio, carbonylated proteins and oxidized peroxiredoxin-6 was observed, in addition to MnSOD and TRX1 overexpression in the siRNA DC cells.
  • Likewise, high PARylation levels and high PARP1 protein expression were detected.
  • In contrast, the silenced TINF2 cells did not alter any evaluated oxidative stress marker.
  • Altogether these findings lead us to conclude that loss of DKC1 and NOP10 functions induces oxidative stress in a telomere shortening independent manner.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
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  • (PMID = 29055871.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Aging / Antioxidant / DNA damage / Oxidative stress / Telomeropathies
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6. Ikeda M, Ishima Y, Kinoshita R, Chuang VTG, Tasaka N, Matsuo N, Watanabe H, Shimizu T, Ishida T, Otagiri M, Maruyama T: A novel S-sulfhydrated human serum albumin preparation suppresses melanin synthesis. Redox Biol; 2018 Apr;14:354-360

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel S-sulfhydrated human serum albumin preparation suppresses melanin synthesis.
  • Products of ultraviolet (UV) irradiation such as reactive oxygen species (ROS) and nitric oxide (NO) stimulate melanin synthesis.
  • Reactive sulfur species (RSS) have been shown to have strong ROS and NO scavenging effects.
  • However, the instability and low retention of RSS limit their use as inhibitors of melanin synthesis.
  • The free thiol at Cys34 on human serum albumin (HSA) is highly stable, has a long retention and possess a high reactivity for RSS.
  • We report herein on the development of an HSA based RSS delivery system.
  • Sulfane sulfur derivatives released from sodium polysulfides (Na<sub>2</sub>S<sub>n</sub>) react readily with HSA.
  • An assay for estimating the elimination of sulfide from polysulfide showed that almost all of the sulfur released from Na<sub>2</sub>S<sub>n</sub> bound to HSA.
  • The Na<sub>2</sub>S<sub>n</sub>-treated HSA was found to efficiently scavenge ROS and NO produced from chemical reagents.
  • The Na<sub>2</sub>S<sub>n</sub>-treated HSA was also found to inhibit melanin synthesis in B16 melanoma cells and this inhibition was independent of the number of added sulfur atoms.
  • In B16 melanoma cells, the Na<sub>2</sub>S<sub>n</sub>-treated HSA also inhibited the levels of ROS and NO induced by UV radiation.
  • Finally, the Na<sub>2</sub>S<sub>n</sub>-treated HSA inhibited melanin synthesis from L-DOPA and mushroom tyrosinase and suppressed the extent of aggregation of melanin pigments.
  • These data suggest that Na<sub>2</sub>S<sub>n</sub>-treated HSA inhibits tyrosinase activity for melanin synthesis via two pathways; by directly inhibiting ROS signaling and by scavenging NO.
  • These findings indicate that Na<sub>2</sub>S<sub>n</sub>-treated HSA has potential to be an attractive and effective candidate for use as a skin whitening agent.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
  • (PMID = 29040960.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Human serum albumin / Oxidative stress / Reactive sulfur species / Ultraviolet irradiation / Whitening agent
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7. Castillo C, Zaror S, Gonzalez M, Hidalgo A, Burgos CF, Cabezas OI, Hugues F, Jiménez SP, González-Horta E, González-Chavarría I, Gavilán J, Montesino R, Sánchez O, Lopez MG, Fuentealba J, Toledo JR: Neuroprotective effect of a new variant of Epo nonhematopoietic against oxidative stress. Redox Biol; 2018 Apr;14:285-294

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroprotective effect of a new variant of Epo nonhematopoietic against oxidative stress.
  • Human erythropoietin is mainly recognized for its hematopoietic function; however, by binding to its receptor (EpoR), it can activate different signaling pathways as STAT, PI3K, MAPK and RAS to increase cellular differentiation or provide neuroprotective effects, among others.
  • A recombinant human erythropoietin variant with low glycosylation and without hematopoietic effect (EpoL) was purified from skimmed goat milk.
  • Recombinant human erythropoietin (Epo) was obtained from CHO cell line and used as control to compare EpoL effects.
  • Neuroprotection studies were performed in PC12 cells and rat hippocampal slices.
  • Cells were pretreated during 1h with EpoL or Epo and exposed to oxidative agents (H<sub>2</sub>O<sub>2</sub> or FCCP); cell viability was assayed at the end of the experiment by the MTT method.
  • Hippocampal slices were exposed to 15min of oxygen and glucose deprivation (OGD) and the neuroprotective drugs EpoL or Epo were incubated for 2h post-OGD in re-oxygenated medium.
  • Cell cultures stressed with oxidative agents, and pretreated with EpoL, showed neuroprotective effects of 30% at a concentration 10 times lower than that of Epo.
  • Moreover, similar differences were observed in OGD ex vivo assays.
  • Neuroprotection elicited by EpoL was lost when an antibody against EpoR was present, indicating that its effect is EpoR-dependent.
  • In conclusion, our results suggest that EpoL has a more potent neuroprotective profile than Epo against oxidative stress, mediated by activation of EpoR, thus EpoL represents an important target to develop a potential biopharmaceutical to treat different central nervous system pathologies related to oxidative stress such as stroke or neurodegenerative diseases.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
  • (PMID = 28987867.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Erythropoietin / Erythropoietin receptor / Neuroprotection / Oxidative stress
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8. Kozuki N, Katz J, Englund JA, Steinhoff MC, Khatry SK, Shrestha L, Kuypers J, Mullany LC, Chu HY, LeClerq SC, Tielsch JM: Impact of maternal vaccination timing and influenza virus circulation on birth outcomes in rural Nepal. Int J Gynaecol Obstet; 2018 Jan;140(1):65-72

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of maternal vaccination timing and influenza virus circulation on birth outcomes in rural Nepal.
  • OBJECTIVE: To describe the effect of maternal vaccination on birth outcomes in rural Nepal, modified by timing of vaccination in pregnancy and influenza virus activity.
  • METHODS: A secondary analysis was conducted using data from two annual cohorts of a randomized controlled trial.
  • A total of 3693 pregnant women from Sarlahi District were enrolled between April 25, 2011, and September 9, 2013.
  • All participants were aged 15-40 years and received a trivalent inactivated influenza vaccine or placebo.
  • The outcome measures included birth weight, pregnancy length, low birth weight (<2500 g), preterm birth, and small-for-gestational-age birth.
  • RESULTS: Data were available on birth weight for 2741 births and on pregnancy length for 3623 births.
  • Maternal vaccination increased mean birthweight by 42 g (95% confidence interval [CI] 8-76).
  • The magnitude of this increase varied by season but was greatest among pregnancies with high influenza virus circulation during the third trimester.
  • Birth weight increased by 111 g (95% CI -51 to 273) when 75%-100% of a pregnancy's third trimester had high influenza virus circulation versus 38 g (95% CI -6 to 81) when 0%-25% of a pregnancy's third trimester had high influenza virus circulation.
  • However, these results were nonsignificant.
  • CONCLUSION: Seasonal maternal influenza vaccination in rural Nepal increased birth weight; the magnitude appeared larger during periods of high influenza virus circulation.
  • CLINICALTRIALS.GOV: NCT01034254.

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  • [Copyright] © 2017 The Authors. International Journal of Gynecology & Obstetrics published by John Wiley & Sons Ltd on behalf of International Federation of Gynecology and Obstetrics.
  • (PMID = 28984909.001).
  • [ISSN] 1879-3479
  • [Journal-full-title] International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics
  • [ISO-abbreviation] Int J Gynaecol Obstet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Influenza / Low birth weight / Nepal / Pregnancy / Preterm / Small for gestational age / Vaccination
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9. Soria F, Marra G, Čapoun O, Soukup V, Gontero P: Prevention of bladder cancer incidence and recurrence: tobacco use. Curr Opin Urol; 2018 Jan;28(1):80-87

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevention of bladder cancer incidence and recurrence: tobacco use.
  • PURPOSE OF REVIEW: To summarize the current knowledge about smoking carcinogenesis in bladder cancer (BCa), individual susceptibility and impact of smoking on incidence and outcomes of nonmuscle invasive BCa (NMIBC) and muscle-invasive BCa (MIBC).
  • To assess the impact of smoking cessation on oncological outcomes.
  • RECENT FINDINGS: Smoking pattern, intensity, and duration are responsible for an increased risk of developing BCa and for worse tumor features at presentation.
  • Tobacco consumption is associated with a higher risk of recurrence in NMIBC and with an impaired intravesical therapy efficacy.
  • To date, the impact of smoking on oncological outcomes after radical surgery remains unclear.
  • SUMMARY: Smoking cessation decreases the risk of BCa and may also allow benefits on treatment outcomes.
  • Nonetheless, the magnitude of the effect remains unclear and prospective series with the specific aim of weighing smoking cessation on outcomes are needed.
  • Because even a 5-min counseling in the urology setting may be sufficient to significantly enhance smoking cessation rates, adequate knowledge of links between tobacco and BCa, from its molecular pathophysiology and its harms to benefits of cessation is paramount for urologists and for everyday clinical practice.

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  • (PMID = 28984720.001).
  • [ISSN] 1473-6586
  • [Journal-full-title] Current opinion in urology
  • [ISO-abbreviation] Curr Opin Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. Fang CY, Chen JS, Chang SK, Shen CH: Reversine induces autophagic cell death through the AMP-activated protein kinase pathway in urothelial carcinoma cells. Anticancer Drugs; 2018 Jan;29(1):29-39

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reversine induces autophagic cell death through the AMP-activated protein kinase pathway in urothelial carcinoma cells.
  • Urothelial carcinoma is one of the most common malignancies of the urinary tract.
  • Effective treatment of advanced urothelial carcinoma remains a clinical challenge with poor outcomes in these patients.
  • Previous reports have shown that the expression of aurora kinase is associated with clinical stage and prognosis; hence, aurora kinases are potential targets in urothelial carcinoma therapy.
  • Reversine, an aurora kinase inhibitor, was analyzed for its cytotoxicity in this study.
  • Cell proliferation, flow cytometry, western blotting, and immunofluorescent assay were used to determine the effect of reversine on urothelial carcinoma cells.
  • The results showed that reversine significantly inhibits the growth of urothelial carcinoma cell lines.
  • Reversine induced cell cycle arrest at the G2/M phase, leading to autophagic cell death by activating the AMP-activated protein kinase pathway.
  • Reversine induced significant cell death in urothelial carcinoma cells.
  • Our results suggest that reversine may be a suitably small molecule for treating urothelial carcinoma in the future.

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  • (PMID = 28984683.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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