Downregulation of programmed cell death 10 is associated with tumor cell proliferation, hyperangiogenesis and peritumoral edema in human glioblastoma

Lambertz, Nicole; Hindy, Nicolai El; Kreitschmann-Andermahr, Ilonka; Stein, Klaus-Peter; Dammann, Philipp; Oezkan, Neriman; Mueller, Oliver; Sure, Ulrich; Zhu, Yuan

doi:10.1186/s12885-015-1709-8

Cited by 26 publications

(32 citation statements)

References 40 publications

(62 reference statements)

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“…This observation was in accordance with previous findings that revealed that silencing PDCD10 could inhibit the proliferation of endothelial cells (32). Lambertz et al (33) proposed that PDCD10 potentially participated in tumor proliferation, apoptosis, hyper-angiogenesis and peritumoral edema in human glioblastoma. In addition, downregulation of PDCD10 inhibited tumor cell proliferation (33).…”

Section: Discussionsupporting

confidence: 93%

“…Lambertz et al (33) proposed that PDCD10 potentially participated in tumor proliferation, apoptosis, hyper-angiogenesis and peritumoral edema in human glioblastoma. In addition, downregulation of PDCD10 inhibited tumor cell proliferation (33). In addition to the effect on proliferation, previous studies indicated a positive correlation between Figure 6.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionsupporting

confidence: 93%

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 protein extraction and Western blot were performed according to the previously established protocols . The following primary antibodies were used: rabbit anti‐Dll4 (1:1000; Cell Signaling Technology, Frankfurt, Germany), rabbit anti‐cleaved Notch1 (1:500; Cell Signaling Technology), goat anti‐cleaved Notch4 (1:200; Santa Cruz Biotechnology, Sant Cruz, CA, USA), rabbit anti‐Hey1 (1:200; Abcam, Cambridge, UK), mouse anti‐PCNA (1:500; Dako, Hamburg, Germany), rabbit anti‐VEGF (1:500; Santa Cruz Biotechnology), rabbit anti‐CXCR4 (1:500; Abcam), mouse anti‐p‐Akt (Ser473) (1:1000; Cell Signaling Technology), rabbit anti‐p‐Erk1/2 (Thr202/Tyr204 for P‐Erk1; Thr185/Tyr187 for P‐Erk2; 1:1000; Cell Signaling Technology) and rabbit anti‐GAPDH (1:1000; Cell Signaling Technology) as reference protein.…”

Section: Methodsmentioning

confidence: 99%

“…Total protein extraction and Western blot were performed according to the previously established protocols. 22 The following primary antibodies were used: rabbit anti-Dll4 (1:1000; Cell Signaling Technology, Frankfurt, Germany), rabbit anti-…”

Section: Western Blotmentioning

confidence: 99%

Study of angiogenic signaling pathways in hemangioblastoma

et al. 2016

Self Cite

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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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“…Phosphorylated PI3K/Akt inhibits pro-apoptotic substrates, such as CHOP and p-JNK, while it promotes the anti-apoptotic substrate Bcl-2 (21). Recent evidence suggests that PDCD10 is associated with the activation of Akt signaling protein (22). The current study found that miR-613 significantly increased the level of p-Akt and Bcl-2 expression; when miR-613 was overexpressed, however, the level of expression of the pro-apoptotic proteins CHOP and p-JNK decreased significantly.…”

Section: Discussionmentioning

confidence: 99%

miR-613 suppresses ischemia-reperfusion-induced cardiomyocyte apoptosis by targeting the programmed cell death 10 gene

Guo

et al. 2016

BST

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Downregulation of programmed cell death 10 is associated with tumor cell proliferation, hyperangiogenesis and peritumoral edema in human glioblastoma

Cited by 26 publications

References 40 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

miR-613 suppresses ischemia-reperfusion-induced cardiomyocyte apoptosis by targeting the programmed cell death 10 gene

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