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pmid:31761897

Forkhead Box R2 Knockdown Decreases Chemoresistance to Cisplatin via MYC Pathway in Bladder Cancer.

Yangle Li · Xiongbing Zu · Xiheng Hu · Long Wang · Wei He

Medical science monitor : international medical journal of experimental and clinical research · 2019 doi:10.12659/MSM.917345

Paper

complete

Experiment

complete

Data

partial

Analysis

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title
Forkhead Box R2 Knockdown Decreases Chemoresistance to Cisplatin via MYC Pathway in Bladder Cancer.
doi
10.12659/MSM.917345
pmid
31761897
authors array · 5 items
[0]
Yangle Li
[1]
Xiongbing Zu
[2]
Xiheng Hu
[3]
Long Wang
[4]
Wei He
journal
Medical science monitor : international medical journal of experimental and clinical research
year
2019
abstract
BACKGROUND Bladder cancer is a very common urological cancer globally, and cisplatin- or gemcitabine-based chemotherapy is essential for advanced bladder cancer patients. Many patients with bladder cancer have a relatively poor response to chemotherapy, leading to failure of clinical treatment. We mined the GSE77883 GEO dataset, identifying FoxR2 as being a significantly upregulated gene in T24 chemoresistant cells. Herein, we assessed how FoxR2 functions in bladder cancer cell chemoresistance. MATERIAL AND METHODS Cisplatin-resistant T24 (T24/DDP) cells were constructed by administering increasing concentrations of cisplatin, and differences in expression of FoxR2 were examined in T24/DDP and T24 cells. FoxR2 loss- and gain-of-function cells models were established in T24/DDP and T24 cells, respectively. Cell survival, clone formation, cell cycle, and cell apoptosis were assessed, and the MYC pathway was verified. RESULTS FoxR2 was significantly upregulated in T24/DDP cells compared to T24 cells. Knockdown of FoxR2 in T24/DDP cells, survival rate, and clone formation were decreased, G1/S phase transition was suppressed, and cell apoptosis was promoted. These results were reversed by restoration of FoxR2 levels in T24 cells. We found that FoxR2 knockdown enhanced sensitivity to cisplatin, whereas MYC overexpression antagonized chemosensitivity in T24/DDP cells. CONCLUSIONS FoxR2 knockdown decreases chemoresistance to cisplatin via the MYC pathway in bladder cancer cells, and this may be a target for overcoming chemoresistance in bladder cancer.
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Data were compared via t tests and one-way ANOVA with Tukey’s multiple comparison test for 2 and >2 groups, respectively.
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Mining of Gene Expression Omnibus (GEO) data for GSE77883 revealed increased expression of FoxR2 in T24-chemoresistant cells compared with parent cells, suggesting that FoxR2 is involved in bladder cancer chemoresistance.
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Mining of Gene Expression Omnibus (GEO) data for GSE77883 revealed increased expression of FoxR2 in T24-chemoresistant cells compared with parent cells, suggesting that FoxR2 is involved in bladder cancer chemoresistance.
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Mining of Gene Expression Omnibus (GEO) data for GSE77883 revealed increased expression of FoxR2 in T24-chemoresistant cells compared with parent cells, suggesting that FoxR2 is involved in bladder cancer chemoresistance.
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Mining of Gene Expression Omnibus (GEO) data for GSE77883 revealed increased expression of FoxR2 in T24-chemoresistant cells compared with parent cells, suggesting that FoxR2 is involved in bladder cancer chemoresistance.
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Enzalutamide inhibits proliferation of gemcitabine-resistant bladder cancer cells with increased androgen receptor expression
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Mining of Gene Expression Omnibus (GEO) data for GSE77883 revealed increased expression of FoxR2 in T24-chemoresistant cells compared with parent cells, suggesting that FoxR2 is involved in bladder cancer chemoresistance.
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Forkhead Box R2 Knockdown Decreases Chemoresistance to Cisplatin via M
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Complete file
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Many patients with bladder cancer have a relatively poor response to chemotherapy, leading to failure of clinical treatment. We mined the GSE77883 GEO dataset, identifying FoxR2 as being a significantly upregulated gene in T24 chemoresistant cells. Herein, we assessed how FoxR2 functions in bladder cancer cell chemoresistance. MATERIAL AND METHODS Cisplatin-resistant T24 (T24/DDP) cells were constructed by administering increasing concentrations of cisplatin, and differences in expression of FoxR2 were examined in T24/DDP and T24 cells. FoxR2 loss- and gain-of-function cells models were established in T24/DDP and T24 cells, respectively. Cell survival, clone formation, cell cycle, and cell apoptosis were assessed, and the MYC pathway was verified. RESULTS FoxR2 was significantly upregulated in T24/DDP cells compared to T24 cells. Knockdown of FoxR2 in T24/DDP cells, survival rate, and clone formation were decreased, G1/S phase transition was suppressed, and cell apoptosis was promoted. These results were reversed by restoration of FoxR2 levels in T24 cells. We found that FoxR2 knockdown enhanced sensitivity to cisplatin, whereas MYC overexpression antagonized chemosensitivity in T24/DDP cells. 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