Loss of endothelial programmed cell death 10 activates glioblastoma cells and promotes tumor growth

Zhu, Yuan; Zhao, Kai; Prinz, Anja; Keyvani, Kathy; Lambertz, Nicole; Kreitschmann-Andermahr, Ilonka; Lei, Ting; Sure, Ulrich

doi:10.1093/neuonc/nov155

Cited by 33 publications

(44 citation statements)

References 34 publications

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“…Synthetic biological functions of PDCD10 warrant more investigation. In contrast to the well-established mechanism of PDCD10 in vessel permeability and neo-angiogenesis, limited information about PDCD10 in cancer research has been reported (35,36). He et al (37) forecasted that PDCD10 may play an important role in cancer since it can influence angiogenesis by targeting vascular endothelial growth factor receptor 2 (VEGFR2) (37).…”

Section: Discussionmentioning

confidence: 99%

miRNA‑26a‑5p and miR‑26b‑5p inhibit the proliferation of bladder cancer cells by regulating PDCD10

Jiang

et al. 2018

Oncol Rep

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MicroRNA (miR)-26a-5p and miR-26b-5p consistently play an antitumor role in many types of cancers, but the underlying mechanism remains unclear in bladder cancer (BC). In the present study, we found that, in BC tissues, the levels of miR-26a-5p and miR-26b-5p were lower than in paired normal tissues. The upregulation of miR-26-5p significantly inhibited the proliferation of BC cell lines (T24 and 5637). Bioinformatics analysis indicated that Programmed Cell Death 10 (PDCD10) was the downstream target gene of miR-26a-5p/miR-26b-5p, and this was ascertained by western blotting and quantitative real-time reverse transcription PCR (RT-qPCR). In addition, in the 3'-UTR of PDCD10, the binding site was identified using a luciferase reporter assay. We determined that clinical BC tissues presented higher PDCD10 levels than adjacent normal tissues and that PDCD10 promoted proliferation of BC cell lines. Overexpression of miR-26a-5p/miR-26b-5p inhibited the stimulatory effect on proliferation of BC cells induced by PDCD10. In addition, in vivo experiments and clinical data revealed that the prognosis of BC patients with high expression of miR-26a-5p/miR-26b-5p and low expression of PDCD10 was better than that of patients with low miR-26-5p and high PDCD10 expression. These data revealed that miR-26a-5p and miR-26b-5p were pivotal regulators in BC progression by targeting the proliferation-related protein, PDCD10. The miR-26-5p/PDCD10 interaction may provide important insight into the pathway of BC progression and present novel opportunities for future diagnosis and treatment strategies, especially for patients with high levels of PDCD10.

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Section: Discussionmentioning

confidence: 99%

miRNA‑26a‑5p and miR‑26b‑5p inhibit the proliferation of bladder cancer cells by regulating PDCD10

Jiang

et al. 2018

Oncol Rep

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“…Total RNA extraction, cDNA synthesis and RT 2 ‐PCR were performed as previously described . The primers and the annealing temperature for individual genes are listed in Table (Supporting Information).…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA extraction, cDNA synthesis and real-time RT-PCR (RT 2 -PCR) Total RNA extraction, cDNA synthesis and RT 2 -PCR were performed as previously described. 20 The primers and the D Pierscianek et al…”

Section: Patientsmentioning

confidence: 99%

Study of angiogenic signaling pathways in hemangioblastoma

et al. 2016

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Hemangioblastoma (HB) is mainly located in the brain and the spinal cord. The tumor is composed of two major components, namely neoplastic stromal cells and abundant microvessels. Thus, hyper-vascularization is the hallmark of this tumor. Despite the identification of germline and/or epigenetic mutations of Von Hippel Lindau (VHL) gene as an important pathogenic mechanism of HB, little is known about the molecular signaling involved in this highly vascularized tumor. The present study investigated the key players of multiple angiogenic signaling pathways including VEGF/VEGFR2, EphB4/EphrinB2, SDF1α/CXCR4 and Notch/Dll4 pathways in surgical specimens of 22 HB. The expression of key angiogenic factors was detected by RT -PCR and Western blot. Immunofluorescent staining revealed the cellular localization of these proteins. We demonstrated a massive upregulation of mRNA levels of VEGF and VEGFR2, CXCR4 and SDF1α, EphB4 and EphrinB2, as well as the main components of Dll4-Notch signaling in HB. An increase in the protein expression of VEGF, CXCR4 and the core-components of Dll4-Notch signaling was associated with an activation of Akt and Erk1/2 and accompanied by an elevated expression of PCNA. Immuofluorescent staining revealed the expression of VEGF and CXCR4 in endothelial cells as well as in tumor cells. Dll4 protein was predominantly found in tumor cells, whereas EphB4 immunoreactivity was exclusively detected in endothelial cells. We conclude that multiple key angiogenic pathways were activated in HB, which may synergistically contribute to the abundant vascularization in this tumor. Identification of these aberrant pathways provides potential targets for a possible future application of anti-angiogenic therapy for this tumor, particularly when a total surgical resection becomes difficult due to the localization or multiplicity of the tumor.

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“…Table 1 Recently discovered pro-and anti-angiogenesis factors Pro-angiogenesis TGLI1 [63], H19 [51], C/EBPbeta [14], MCSF [15], annexin A2 [39], CXCR4 [66], Oct-3/4 [16], miR-31 [50], miR-148a, HSP47 [38] Anti-angiogenesis hHSS1 [29], NNC55-0396 [30], TTAC-0001 [67], calpastatin [68], miR-137 [65], EZH2 [65], BMP7v [31], PDCD10 [32], JSI-124 [33] Brain Tumor Pathol…”

Section: Resultsmentioning

confidence: 99%

“…Because of the loss of programmed cell death 10 (PDCD10), some proangiogenic factors decreased. It is credible that PDCD10 may show anti-angiogenesis-like function in GBM [32]. Moreover, JSI-124 is demonstrated effectively to inhibit GBM angiogenesis and invasion [33].…”

Section: Angiogenesis In Gbm and Anti-angiogenic Therapiesmentioning

confidence: 97%

Recent advance in molecular angiogenesis in glioblastoma: the challenge and hope for anti-angiogenic therapy

Zhang

et al. 2015

Brain Tumor Pathol

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Glioblastoma (GBM) is the most highly malignant brain tumor in the human central nerve system. In this paper, we review new and significant molecular findings on angiogenesis and possible resistance mechanisms. Expression of a number of genes and regulators has been shown to be upregulated in GBM microvessel cells, such as interleukin-8, signal transducer and activator of transcription 3, Tax-interacting protein-1, hypoxia induced factor-1 and anterior gradient protein 2. The regulator factors that may strongly promote angiogenesis by promoting endothelial cell metastasis, changing the microenvironment, enhancing the ability of resistance to anti-angiogenic therapy, and that inhibit angiogenesis are reviewed. Based on the current knowledge, several potential targets and strategies are proposed for better therapeutic outcomes, such as its mRNA interference of DII4-Notch signaling pathway and depletion of b1 integrin expression. We also discuss possible mechanisms underlying the resistance to anti-angiogenesis and future directions and challenges in developing new targeted therapy for GBM.

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Loss of endothelial programmed cell death 10 activates glioblastoma cells and promotes tumor growth

Cited by 33 publications

References 34 publications

miRNA‑26a‑5p and miR‑26b‑5p inhibit the proliferation of bladder cancer cells by regulating PDCD10

miRNA‑26a‑5p and miR‑26b‑5p inhibit the proliferation of bladder cancer cells by regulating PDCD10

Study of angiogenic signaling pathways in hemangioblastoma

Recent advance in molecular angiogenesis in glioblastoma: the challenge and hope for anti-angiogenic therapy

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