OSU‐T315 and doxorubicin synergistically induce apoptosis via mitochondrial pathway in bladder cancer cells

Li, Zhihui; Ren, Danhong; Chen, Chen; Sun, Leiming; Fang, Kun

doi:10.1002/cbin.11855

Cited by 5 publications

(2 citation statements)

References 29 publications

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“…DOX be-longs to the anthracycline class of antibiotics and integrates with the DNA of the cell nucleus, disrupting the DNA structure and causing apoptosis and cell growth arrest. However, DOX resistance is also a barrier to failed therapy [23].…”

Section: Discussionmentioning

confidence: 99%

EIF5A2 Promotes Doxorubicin Resistance in Bladder Cancer Cells through the TGF-β Signaling Pathway

Yang,

Jiang,

Chen

et al. 2023

Discovery Medicine

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Background: Doxorubicin (DOX) is a commonly used chemotherapeutic agent, but bladder cancer (BC) patients often develop resistance that limits therapeutic efficacy. Recent research has demonstrated a link between medication resistance and the expression of eukaryotic translation initiation factor 5A2 (EIF5A2) in tumors. This study aimed to investigate whether EIF5A2 affects the resistance of BC cells to doxorubicin through the transforming growth factor (TGF)-β signaling pathway. Methods: Doxorubicin-resistant cells in BC (T24/DOX and 5637/DOX) were constructed, then cell viability was detected by cell counting kit-8 (CCK-8); EIF5A2 mRNA expression was detected using quantitative real-time PCR (qRT-PCR); cell proliferation was detected using clone formation; apoptosis was detected by flow cytometry; and finally, proteins related to the TGF-β signaling pathway (EIF5A2, TGF-β1, p-small mothers against decapentaplegic 2 (Smad2)/Smad2, p-Smad3/Smad3) were detected using western blot. Results: EIF5A2 was up-regulated in DOX-resistant BC cells, and DOX intervention promoted proliferation and inhibited apoptosis in DOX-resistant BC cells. si-EIF5A2 reversed the above effects. EIF5A2 resulted in DOX resistance by activating the TGF-β pathway, and the TGF-β activator SRI-011381 reversed the inhibitory effect of si-EIF5A2 on DOX resistance. Conclusions: EIF5A2 promotes DOX resistance in BC cells through the TGF-β signaling pathway, and EIF5A2 may be a potential counter-resistance therapeutic strategy in BC chemotherapy.

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Section: Discussionmentioning

confidence: 99%

EIF5A2 Promotes Doxorubicin Resistance in Bladder Cancer Cells through the TGF-β Signaling Pathway

Yang,

Jiang,

Chen

et al. 2023

Discovery Medicine

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“…Stevioside was identified by high-throughput screening as a useful compound to increase cell apoptosis via activation of GSK-3b and induction of FBXW7, contributing to downregulation of MCL-1 in bladder cancer (139). Similarly, OSU-T315, an inhibitor of integrinlinked kinase, was observed to inhibit Mcl-1 expression levels via targeting the GSK-3b/FBXW7 axis in bladder cancer cells (140). Green tea polyphenol EGCG plays a tumor suppressive role in bladder cancer via inactivation of NF-kappa B.…”

Section: Compounds Regulate E3 Ligases In Bladder Cancermentioning

confidence: 99%

The role of E3 ubiquitin ligases and deubiquitinases in bladder cancer development and immunotherapy

Wang

Zhang

et al. 2023

Front. Immunol.

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Bladder cancer is one of the common malignant urothelial tumors. Post-translational modification (PTMs), including ubiquitination, acetylation, methylation, and phosphorylation, have been revealed to participate in bladder cancer initiation and progression. Ubiquitination is the common PTM, which is conducted by E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme and E3 ubiquitin-protein ligase. E3 ubiquitin ligases play a key role in bladder oncogenesis and progression and drug resistance in bladder cancer. Therefore, in this review, we summarize current knowledge regarding the functions of E3 ubiquitin ligases in bladder cancer development. Moreover, we provide the evidence of E3 ubiquitin ligases in regulation of immunotherapy in bladder cancer. Furthermore, we mention the multiple compounds that target E3 ubiquitin ligases to improve the therapy efficacy of bladder cancer. We hope our review can stimulate researchers and clinicians to investigate whether and how targeting E3 ubiquitin ligases acts a novel strategy for bladder cancer therapy.

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Molecular and cellular mechanisms of chemoresistance in paediatric pre–B cell acute lymphoblastic leukaemia

Lill,

Fitter,

Zannettino

et al. 2024

Cancer Metastasis Rev

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Paediatric patients with relapsed B cell acute lymphoblastic leukaemia (B-ALL) have poor prognosis, as relapse-causing clones are often refractory to common chemotherapeutics. While the molecular mechanisms leading to chemoresistance are varied, significant evidence suggests interactions between B-ALL blasts and cells within the bone marrow microenvironment modulate chemotherapy sensitivity. Importantly, bone marrow mesenchymal stem cells (BM-MSCs) and BM adipocytes are known to support B-ALL cells through multiple distinct molecular mechanisms. This review discusses the contribution of integrin-mediated B-ALL/BM-MSC signalling and asparagine supplementation in B-ALL chemoresistance. In addition, the role of adipocytes in sequestering anthracyclines and generating a BM niche favourable for B-ALL survival is explored. Furthermore, this review discusses the role of BM-MSCs and adipocytes in promoting a quiescent and chemoresistant B-ALL phenotype. Novel treatments which target these mechanisms are discussed herein, and are needed to improve dismal outcomes in patients with relapsed/refractory disease.

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OSU‐T315 and doxorubicin synergistically induce apoptosis via mitochondrial pathway in bladder cancer cells

Cited by 5 publications

References 29 publications

EIF5A2 Promotes Doxorubicin Resistance in Bladder Cancer Cells through the TGF-β Signaling Pathway

EIF5A2 Promotes Doxorubicin Resistance in Bladder Cancer Cells through the TGF-β Signaling Pathway

The role of E3 ubiquitin ligases and deubiquitinases in bladder cancer development and immunotherapy

Molecular and cellular mechanisms of chemoresistance in paediatric pre–B cell acute lymphoblastic leukaemia

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