Erythropoietin Promotes Glioblastoma via miR-451 Suppression

Alural, Begüm; Ayyildiz, Zeynep Ozge; Tüfekci, Kemal Uğur; Genç, Şermin

doi:10.1016/bs.vh.2017.03.002

Cited by 14 publications

(9 citation statements)

References 53 publications

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“…The present study presented experimental evidence demonstrating that Epo induces resistance to cisplatin-mediated death in cervical cancer cells. The findings are in accord with previous studies revealing that administration of exogenous Epo mediated acquisition of resistance to cisplatin in glioblastoma (18) and non-small cell lung carcinoma cells (19).…”

Section: Discussionsupporting

confidence: 92%

Erythropoietin promotes expression of survivin via STAT3 activation and reduces sensitivity to cisplatin in cervical cancer cells

et al. 2018

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Erythropoietin (Epo) is used for the treatment of cancer-associated anaemia. However, certain studies have identified that the administration of Epo mediates the acquisition of resistance to cisplatin, which is widely used to treat cervical cancer. Our group previously reported that cervical cancer cells express Epo receptor and that exogenous Epo induces cell proliferation and migration. However, the effect of Epo on cervical cancer cell death mediated by chemotherapeutic agents has not yet been evaluated. Thus, the aim of the present study was to assess the potential effect of Epo on the cytotoxic activity of cisplatin in cervical cancer cells. The effect of Epo was assessed in 3 cervical cancer-derived cell lines. It was observed that pre-incubation with Epo induced a significant reduction of cisplatin-induced apoptosis in vitro and in vivo. Incubation with Epo induced the expression and activation of the transcriptional factor signal transducer and activator of transcription 3 (STAT3), which in turn stimulated the expression and activation of the anti-apoptotic protein survivin. The cytotoxicity of cisplatin was partially restored by treating the cells with MY155, an inhibitor of survivin. Conversely, inhibition of STAT3 activation using sub-lethal doses of WP1066, completely abolished the cytoprotective effect of Epo. These observations indicated that Epo was able to hinder the cytotoxic effect of cisplatin in cervical cancer cells by activating anti-apoptotic responses regulated by STAT3.

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Section: Discussionsupporting

confidence: 92%

Erythropoietin promotes expression of survivin via STAT3 activation and reduces sensitivity to cisplatin in cervical cancer cells

et al. 2018

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“…Besides, miR-451 acted as a tentative switch in mediating glioma cells growth and migration [20][21][22]. Thus, targeting miR-451 has been regarded as a potential adjuvant therapy for glioma besides chemotherapy [23]. In this study, whether miR-451 is related to LSINCT5 in glioma cells is studied.…”

Section: Introductionmentioning

confidence: 96%

Knockdown of lncRNA LSINCT5 suppresses growth and metastasis of human glioma cells via up-regulating miR-451

Liu

Cao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Glioma is a main cause of brain-cancer relevant death. The present paper designed to reveal the possible role of LSINCT5 in human glioma GL15 cells. Methods: LSINCT5 and miR-451 expression in glioma tissues was examined using qRT-PCR. The impacts of LSINCT5, miR-451 and Rac1 in GL15 cells were checked by carrying out CCK-8 assay, transwell assay, and flow cytometric analysis. Further, the target gene of LSINCT5 and miR-451 was explored. Accumulation of PI3K/AKT, Wnt/b-catenin and NF-jB pathway proteins was examined using Western blot. Results: LSINCT5 was highly expressed while miR-451 low expressed in glioma tissues when compared to normal controls. Down-regulating LSINCT5 effectively declined GL15 cells viability, migration and invasion, but accelerated apoptosis. Nonetheless, the above-mentioned effects of LSINCT5 down-regulation were weakened when miR-451 was silenced. Rac1 was a target of miR-451. The tumour-suppressive effects of miR-451 on GL15 cells were weakened when Rac1 was overexpressed. Further, LSINCT5-miR-451-Rac1 axis could impact the activation of PI3K/AKT, Wnt/b-catenin and NF-jB pathways. Conclusion: Down-regulation of LSINCT5 represses glioma cells growth and metastasis in vitro likely through targeting miR-451 and thereby inhibiting Rac1-regulated PI3K/AKT, Wnt/b-catenin and NF-jB pathways.

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“…MiR-451 inhibited the migration and invasion in vitro, as well as in vivo metastasis of hepatocellular carcinoma cells through regulating epithelial-mesenchymal transition process [72]. Importantly, Alural and colleagues demonstrated that suppression of basal levels of miR-451 in GBM cells led to increased cell migration and invasion [73]. These results underscore the relevance of miR-451 overexpression strategy as strong anti-invasive tool that do not alter significantly other phenotypic readouts of GBM cells.…”

Section: Resultsmentioning

confidence: 99%

“…Imatinib and miR-451 alone had no significant effect on GBM neurosphere formation, but in combination, led to its marked inhibition [75]. Erythropoietin-induced suppression of miR-451 in GBM led to increased cisplatin chemoresistance [73]. Overexpression of miR-451 sensitized lung cancer cells to cisplatin [76,77,78] and irradiation [79], breast cancer cells to tamoxifen and paclitaxel [80,81], and colorectal cancer cells to irinotecan [82].…”

Section: Resultsmentioning

confidence: 99%

MicroRNA-451 Inhibits Migration of Glioblastoma while Making It More Susceptible to Conventional Therapy

Ogawa

Ansari

Nowicki

et al. 2019

ncRNA

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Malignant glioblastoma (GBM, glioma) is the most common and aggressive primary adult brain tumor. The prognosis of GBM patients remains poor, despite surgery, radiation and chemotherapy. The major obstacles for successful remedy are invasiveness and therapy resistance of GBM cells. Invasive glioma cells leave primary tumor core and infiltrate surrounding normal brain leading to inevitable recurrence, even after surgical resection, radiation and chemotherapy. Therapy resistance allowing for selection of more aggressive and resistant sub-populations including GBM stem-like cells (GSCs) upon treatment is another serious impediment to successful treatment. Through their regulation of multiple genes, microRNAs can orchestrate complex programs of gene expression and act as master regulators of cellular processes. MicroRNA-based therapeutics could thus impact broad cellular programs, leading to inhibition of invasion and sensitization to radio/chemotherapy. Our data show that miR-451 attenuates glioma cell migration in vitro and invasion in vivo. In addition, we have found that miR-451 sensitizes glioma cells to conventional chemo- and radio-therapy. Our data also show that miR-451 is regulated in vivo by AMPK pathway and that AMPK/miR-451 loop has the ability to switch between proliferative and migratory pattern of glioma cells behavior. We therefore postulate that AMPK/miR-451 negative reciprocal feedback loop allows GBM cells/GSCs to adapt to tumor “ecosystem” by metabolic and behavioral flexibility, and that disruption of such a loop reduces invasiveness and diminishes therapy resistance.

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Erythropoietin Promotes Glioblastoma via miR-451 Suppression

Cited by 14 publications

References 53 publications

Erythropoietin promotes expression of survivin via STAT3 activation and reduces sensitivity to cisplatin in cervical cancer cells

Erythropoietin promotes expression of survivin via STAT3 activation and reduces sensitivity to cisplatin in cervical cancer cells

Knockdown of lncRNA LSINCT5 suppresses growth and metastasis of human glioma cells via up-regulating miR-451

MicroRNA-451 Inhibits Migration of Glioblastoma while Making It More Susceptible to Conventional Therapy

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