Role of 5‑Aza‑CdR in mitomycin‑C chemosensitivity of T24 bladder cancer cells

Zhang, Hui‐Hui; Huang, Bo; Cao, Yi; Li, Qing; Xu, Hui

doi:10.3892/ol.2017.6853

Cited by 7 publications

(5 citation statements)

References 21 publications

(20 reference statements)

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“…Zhang et al. 52 put forward that 5-Aza-2′-deoxycytidine (5‑Aza‑CdR) increased the effect of mitomycin-C (MMC) on bladder cancer cells via autophagy inhibition; therefore, co-treatment with 5‑Aza‑CdR and MMC resulted in increased apoptosis and cell death.…”

Section: Survival Effects Of Autophagy On Bladder Cancer Cellsmentioning

confidence: 99%

Contrast effects of autophagy in the treatment of bladder cancer

Konac

Kurman

Baltacı

2020

Exp Biol Med (Maywood)

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Bladder cancer is a disease that negatively affects patients’ quality of life, but treatment options have remained unchanged for a long time. Although promising results have been achieved with current bladder cancer treatments, cancer recurrence, progression, and therapy resistance are the most severe problems preventing the efficiency of bladder cancer treatments. Autophagy refers to an evolutionarily conserved catabolic process in which proteins, damaged organelles, and cytoplasmic components are degraded by lysosomal enzymes. Autophagy regulates the therapeutic response to the chemotherapy drugs, thus determining the effect of therapy on cancer cells. Autophagy is a stress-induced cell survival mechanism and its excessive stimulation can cause resistance of tumor cells to therapeutic agents. Depending on the conditions, an increase in autophagy may cause treatment resistance or autophagic cell death, and it is related to important anti-cancer mechanisms, such as apoptosis. Therefore, understanding the roles of autophagy under different conditions is important for designing effective anti-cancer agents. The dual role of autophagy in cancer has attracted considerable attention in respect of bladder cancer treatment. In this review, we summarize the basic characteristics of autophagy, including its mechanisms, regulation, and functions, and we present examples from current studies concerning the dual role of autophagy in bladder cancer progression and therapy. Impact statement Autophagy acts as an intracellular recycling system. Infection and mitochondrial damage, maintaining cellular homeostasis, orchestrating nutrient stress, hypoxia, and oxidative stress are some of the physiological roles associated with autophagy. Autophagy has also context-dependent roles in cancer. Autophagy has a significant impact on tumor initiation and promotion, with both tumor-suppressive and tumor-promoting roles. Unfortunately, conventional systemic chemotherapy for cancer therapy has been reported to have primary limitations such as chemo-resistance of targeted cells. The cytoprotective role of autophagy has been postulated as one of the causes of this resistance. Hence, combination therapy using autophagy inhibitors has recently started to emerge as a noteworthy strategy in the treatment of cancer. Therefore, targeting the autophagy pathways may be a potential therapeutic strategy for addressing cancer progression or therapy resistance in the near future. This review will provide a novel insight to understanding the paradoxical roles of autophagy in tumor suppression and tumor promotion.

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Section: Survival Effects Of Autophagy On Bladder Cancer Cellsmentioning

confidence: 99%

Contrast effects of autophagy in the treatment of bladder cancer

Konac

Kurman

Baltacı

2020

Exp Biol Med (Maywood)

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“…MMC is acting as an linking agent for adverse biological action to another in the cell. For the adverse biological action, MMC is associated with apoptosis stimulation, mutagenesis, and suppression of DNA synthesis (Boamah et al, 2007;Mao, Varoglu, & Sherman, 1999;Zhang, Huang, Cao, Li, & Xu, 2017).…”

Section: Introductionmentioning

confidence: 99%

Antioxidant capacity of Nitraria retusa leaf extracts against mitomycin C-induced genetic toxicity in male mice

Khalil

Ahmed

Kassem

et al. 2019

JoBAZ

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Background: Recently, a great interest in the usage of new derived drugs extracted from plant has been increased to treat and/or prevent several diseases including cancer. Therefore, the present study was conducted to use Nitraria retusa leaf extract to increase the antioxidant activity and reduce the genotoxic activity of chemotherapeutic drugs mitomycin C (MMC) in male mice. Male Swiss albino mice (n = 80) were divided in several experimental groups and treated with single dose of MMC with supplementation of 50 and 100 mg/kg body wt Nitraria retusa leaf extract for several time intervals (3 days, 1 week, and 1 month). Results: This study found that MMC-treated mice observed significant increases in the frequency of chromosomal abnormalities in both cell types including bone marrow and spermatocyte cells, induce the mean values of DNA damage, and decrease the expression values of antioxidant enzyme-related genes (CAT, GPx, and GSTT1) compared with control mice. However, supplementation of MMC-treated mice with Nitraria retusa leaf extract suppressed the harmful impacts induced by MMC especially with the high dose and longer duration of the administration. Conclusion: The results suggested that the protective capacity of the Nitraria retusa leaf extract in protecting the hepatic cells could be attributed to the presence of isorhamnetin 3-o-robinobioside, palmitic acid, and β-sitosterols in its extract which are known for their anti-tumor and anti-mutagenic activities.

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“…Further investigation revealed that the autophagy inhibitor ROC-325 improved the anti-leukemic action of azacitidine in acute myeloid leukemia cells [42]. Interestingly, detacibine, an analogue of azacitidine, had a similar effect, as it induced autophagy of cancer cells, including UBUC cells [43,44]. The autophagy-inducing effect of detacibine was observed in mouse neuronal cell lines, which also showed increased hypoxia tolerance following detacibine treatment.…”

Section: Discussionmentioning

confidence: 98%

Intravesical Instillation of Azacitidine Suppresses Tumor Formation through TNF-R1 and TRAIL-R2 Signaling in Genotoxic Carcinogen-Induced Bladder Cancer

Wang

Chang

et al. 2021

Cancers

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Azacitidine, an inhibitor of DNA methylation, shows therapeutic effects against several malignancies by inducing apoptosis and inhibiting tumor cell proliferation. However, the anti-tumor effects of azacitidine on urinary bladder urothelial carcinoma (UBUC), especially following intravesical instillation (IVI), are not established. Here, UBUC cell lines were used to analyze the in vitro therapeutic effects of azacitidine. Potential signaling pathways were investigated by antibody arrays and Western blotting. The N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced rat UBUC model was used for in vivo quantitative analysis of tumor burden. Azacitidine significantly inhibited DNMT expression in UBUC cell lines and reduced cell viability and clonogenic activity, as determined by MTT and colony formation assays, while also inducing significant cytotoxic effects in the form of increased sub-G1 and Annexin V-PI populations (all p < 0.05). Antibody arrays confirmed the in vitro suppression of TNF-R1 and the induction of TRAIL-R2 and their downstream signaling molecules. TNF-R1 suppression reduced claspin and survivin expression, while TRAIL-R2 activation induced cytochrome C and caspase 3 expression. Rats with BBN-induced bladder cancer had a significantly reduced tumor burden and Ki67 index following IVI of azacitidine (p < 0.01). Our study provides evidence for a reduction in BBN-induced bladder cancer by IVI of azacitidine through alterations in the TRAIL-R2 and TNF-R1 signaling pathways. These findings might provide new insights for further clinical trials.

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Role of 5‑Aza‑CdR in mitomycin‑C chemosensitivity of T24 bladder cancer cells

Cited by 7 publications

References 21 publications

Contrast effects of autophagy in the treatment of bladder cancer

Contrast effects of autophagy in the treatment of bladder cancer

Antioxidant capacity of Nitraria retusa leaf extracts against mitomycin C-induced genetic toxicity in male mice

Intravesical Instillation of Azacitidine Suppresses Tumor Formation through TNF-R1 and TRAIL-R2 Signaling in Genotoxic Carcinogen-Induced Bladder Cancer

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