The miR-92b functions as a potential oncogene by targeting on Smad3 in glioblastomas

Wu, Zhe Bao; Cai, Lin; Lin, Shao Jian; Lu, Jiang; Yu, Yao; Zhou, Liang

doi:10.1016/j.brainres.2013.07.031

Cited by 62 publications

(55 citation statements)

References 39 publications

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“…The deregulation of miR-92b has been implicated in several different types of human cancer and serves an oncogenic role (21–23). For instance, miR-92b directly targets PTEN, promotes cell growth and induces cisplatin chemosensitivity in non-small cell lung cancer (NSCLC) cells (21).…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf‑related protein 3

Zhou

Feng

et al. 2017

Exp Ther Med

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Deregulation of microRNA-92b (miR-92b) has been implicated in osteosarcoma. However, the underlying regulatory mechanism of miR-92b in osteosarcoma growth and metastasis remains largely unclear. In the present study, reverse transcription-quantitative polymerase chain reaction and western blotting were used to measure mRNA and protein expression. MTT and Transwell assays were conducted to determine cell proliferation and invasion, and a luciferase reporter assay was performed to confirm the association between miR-92b and Dickkopf3-related protein (DKK3). The results demonstrated that miR-92b was significantly upregulated in osteosarcoma tissues compared with matched adjacent non-tumor tissues. Additionally, high miR-92b levels were significantly associated with lung metastasis and advanced tumor, node, metastasis stage (P<0.05) but not with age, sex, tumor size, location, serum lactate dehydrogenase or serum alkaline phosphatase. miR-92b expression was also significantly upregulated in osteosarcoma cell lines compared with normal osteoblast cells. Knockdown of miR-92b significantly inhibited the proliferation and invasion of osteosarcoma U2OS cells (P<0.01). By contrast, overexpression of miR-92b significantly increased U2OS cell proliferation and invasion (P<0.01). DKK3 was identified as a target gene of miR-92b and it was demonstrated that DKK3 expression was negatively regulated by miR-92b in U2OS cells. Restoration of DKK3 expression abrogated the increased proliferation and invasion of U2OS cells induced by miR-92b overexpression. Notably, DKK3 was significantly downregulated in osteosarcoma tissues compared with adjacent non-tumor tissues and its expression was inversely correlated to miR-92b levels in osteosarcoma tissues. Taken together, these data indicate that miR-92b promotes cell proliferation and invasion in osteosarcoma by targeting DKK3. Therefore, miR-92b may become a potential therapeutic target for osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

“…Inhibition of miR-92b suppresses NSCLC cell growth and motility by targeting RECK (22). Additionally, miR-92b functions as a potential oncogene in glioblastomas by targeting SMAD3 (23). However, the underlying regulatory mechanism of miR-92b in osteosarcoma growth and metastasis remains largely unclear.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf‑related protein 3

Zhou

Feng

et al. 2017

Exp Ther Med

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“…Downregulation of these miRNAs increases expression of PTEN and decreases the level of phosphorylated AKT [26, 27]. Expression of both miR-92b and miR-494-3p is significantly increased in GBM tissues compared to normal brain tissues [27, 28]. Of note, loss of chromosome 10 resulting in the lack of PTEN has also been found in several GSCs lines [29].…”

Section: Akt Signaling In Gbmmentioning

confidence: 99%

AKT/GSK3β Signaling in Glioblastoma

Majewska

Szeliga

2016

Neurochem Res

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Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, survival, migration and resistance to treatment has been implicated in pathogenesis of GBM. One of these pathways is phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT)/rapamycin-sensitive mTOR-complex (mTOR) pathway, intensively studied and widely described so far. Much less attention has been paid to the role of glycogen synthase kinase 3 β (GSK3β), a target of AKT. In this review we focus on the function of AKT/GSK3β signaling in GBM.

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“…For example, Zhe Bao Wu et al showed that local administration of antimir-92b in a subcutaneous U87-MG xenograft mouse model led to the downregulation of Smad3 (a miR-92b target gene) and a decrease in tumor burden [78]. However, the presence of ribonucleases greatly reduces the duration of the RNAi knockdown effects.…”

Section: Assessing Rnai Delivery For Gbm Treatmentmentioning

confidence: 99%

RNA interference for glioblastoma therapy: Innovation ladder from the bench to clinical trials

2017

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Glioblastoma multiforme (GBM) is the most common and deadliest type of primary brain tumor with a prognosis of 14 months after diagnosis. Current treatment for GBM patients includes “total” tumor resection, temozolomide-based chemotherapy, radiotherapy or a combination of these options. Although, several targeted therapies, gene therapy, and immunotherapy are currently in the clinic and/or in clinical trials, the overall survival of GBM patients has hardly improved over the last two decades. Therefore, novel multitarget modalities are urgently needed. Recently, RNA interference (RNAi) has emerged as a novel strategy for the treatment of most cancers, including GBM. RNAi-based therapies consist of using small RNA oligonucleotides to regulate protein expression at the post-transcriptional level. Despite the therapeutic potential of RNAi molecules, systemic limitations including short circulatory stability and low release into the tumor tissue have halted their progress to the clinic. The effective delivery of RNAi molecules through the blood-brain barrier (BBB) represents an additional challenge. This review focuses on connecting the translational process of RNAi-based therapies from in vitro evidence to pre-clinical studies. We delineate the effect of RNAi in GBM cell lines, describe their effectiveness in glioma mouse models, and compare the proposed drug carriers for the effective transport of RNAi molecules through the BBB to reach the tumor in the brain. Furthermore, we summarize the most important obstacles to overcome before RNAi-based therapy becomes a reality for GBM treatment.

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The miR-92b functions as a potential oncogene by targeting on Smad3 in glioblastomas

Cited by 62 publications

References 39 publications

MicroRNA‑92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf‑related protein 3

MicroRNA‑92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf‑related protein 3

AKT/GSK3β Signaling in Glioblastoma

RNA interference for glioblastoma therapy: Innovation ladder from the bench to clinical trials

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