MicroRNA-106a-5p facilitates human glioblastoma cell proliferation and invasion by targeting adenomatosis polyposis coli protein

Li, Dazhi; Wang, Zengliang; Chen, Zigui; Lin, Lin; Wang, Yongxin; Duishanbai, Sailike; Luo, Kun; Du, Guojia; Xiang, Xinggang; Jiafu, Geng Dangmuren

doi:10.1016/j.bbrc.2016.10.132

Cited by 25 publications

(22 citation statements)

References 23 publications

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“…Recently, accumulated studies demonstrated that abnormally expressed miRNAs may act as oncogenes or tumor suppressor genes and is important on the formation and progression of various human cancers, including GBM (34)(35)(36). Therefore, investigation on the expression and roles of miRNAs may have potential tumor diagnostic and prognostic values, as well as therapeutic values for patients with GBM (37).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-543 inhibits proliferation, invasion and induces apoptosis of glioblastoma cells by directly targeting ADAM9

Zhang

2017

Molecular Medicine Reports

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Glioma is the most common type of malignant brain tumor in humans and accounts for 81% of all malignant brain tumor cases in adults. The abnormal expression of microRNAs (miRs) has been reported to be important in the formation and progression of various types of human cancer, including glioblastoma (GBM). Therefore, studies into the expression, and roles of microRNAs as diagnostic and prognostic markers, as well as their therapeutic value for patients with GBM are warranted. The expression and roles of miR‑543 have been reported in several types of human cancer. However, the role of miR‑543 in GBM remains unclear. In the current study, the expression pattern of miR‑543 in GBM, the effects of miR‑543 on GBM cells and the underlying molecular mechanism was determined. The results of the present study demonstrated that miR‑543 was significantly downregulated in GBM tissue samples and cell lines. Furthermore, the upregulation of miR‑543 inhibited GBM cell proliferation and invasion, as well as promoted cell apoptosis. In addition, a disintegrin and metalloproteinase 9 (ADAM9) was identified to be a direct target gene of miR‑543. Furthermore, ADAM9 was significantly upregulated in GBM tissue samples and its expression was inversely correlated with miR‑543 expression in GBM tissue, suggesting that miR‑543 downregulation may contribute to ADAM9 upregulation in GBM. Finally, the results of the rescue experiment indicated that ADAM9 overexpression significantly reversed the effects of miR‑543 on the proliferation, invasion and apoptosis of GBM cells, suggesting that miR‑543 serves as a tumor suppressor in GBM through ADAM9 regulation. Overall, these findings indicate that the miR‑543/ADAM9 signaling pathway may provide as a potential therapeutic strategy for GBM.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-543 inhibits proliferation, invasion and induces apoptosis of glioblastoma cells by directly targeting ADAM9

Zhang

2017

Molecular Medicine Reports

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“…Recent data indicate that increased MIR155HG is associated with glioma grade, mesenchymal transition, and poor prognosis by the generation of its derivatives miR-155-5p and miR-155-3p, which interfere with the activity of protocadherins 9 and 7, respectively, two molecules able to inhibit the Wnt/β-catenin pathway, thereby restraining GBM growth [ 119 ]. In another study, Li et al [ 120 ] pointed out a high expression of miR-106a-5p and an inverse correlation of these levels and APC mRNAs in GBM tissue. Consequently, inhibition of miR-106a-5p expression weakened the invasive ability of this tumor.…”

Section: Alteration Of Wnt Pathways In Glioblastoma Multiforme Andmentioning

confidence: 99%

The Role of Wnt Signal in Glioblastoma Development and Progression: A Possible New Pharmacological Target for the Therapy of This Tumor

Zuccarini

Giuliani

Ziberi

et al. 2018

Genes

100

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Wnt is a complex signaling pathway involved in the regulation of crucial biological functions such as development, proliferation, differentiation and migration of cells, mainly stem cells, which are virtually present in all embryonic and adult tissues. Conversely, dysregulation of Wnt signal is implicated in development/progression/invasiveness of different kinds of tumors, wherein a certain number of multipotent cells, namely “cancer stem cells”, are characterized by high self-renewal and aggressiveness. Hence, the pharmacological modulation of Wnt pathway could be of particular interest, especially in tumors for which the current standard therapy results to be unsuccessful. This might be the case of glioblastoma multiforme (GBM), one of the most lethal, aggressive and recurrent brain cancers, probably due to the presence of highly malignant GBM stem cells (GSCs) as well as to a dysregulation of Wnt system. By examining the most recent literature, here we point out several factors in the Wnt pathway that are altered in human GBM and derived GSCs, as well as new molecular strategies or experimental drugs able to modulate/inhibit aberrant Wnt signal. Altogether, these aspects serve to emphasize the existence of alternative pharmacological targets that may be useful to develop novel therapies for GBM.

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“…This observation was connected with activation of WNT signaling pathway by miR-106a which modify β-catenin cellular localization. Furthermore, miR-106a by facilitation of binding the β-catenin to the promoter regions, enhanced transcription of MMP2 , NANOG , and MYC , as well as genes related to cell invasion RUNX2 , CD44 , SOX9 and OCT4 [ 71 ].…”

Section: Mir-17-92 Mir-106b-25 and Mir-106a-363 In Brain Tumorsmentioning

confidence: 99%

The Oncogenic Relevance of miR-17-92 Cluster and Its Paralogous miR-106b-25 and miR-106a-363 Clusters in Brain Tumors

Gruszka

Zakrzewska

2018

IJMS

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The fundamental function of ribonucleic acids is to transfer genetic information from DNA to protein during translation process, however, this is not the only way connecting active RNA sequences with essential biological processes. Up until now, many RNA subclasses of different size, structure, and biological function were identified. Among them, there are non-coding single-stranded microRNAs (miRNAs). This subclass comprises RNAs of 19–25 nucleotides in length that modulate the activity of well-defined coding RNAs and play a crucial role in many physiological and pathological processes. miRNA genes are located both in exons, introns, and also within non-translated regions. Several miRNAs that are transcribed from the adjacent miRNA genes are called cluster. One of the largest ones is miR-17-92 cluster known as OncomiR-1 due to its strong link to oncogenesis. Six miRNAs from the OncomiR-1 have been shown to play important roles in various physiological cellular processes but also through inhibition of cell death in many cancer-relevant processes. Due to the origin and similarity of the sequence, miR-17-92 cluster and paralogs, miR-106b-25 and miR-106a-363 clusters were defined. Here we discuss the oncogenic function of those miRNA subgroups found in many types of cancers, including brain tumors.

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MicroRNA-106a-5p facilitates human glioblastoma cell proliferation and invasion by targeting adenomatosis polyposis coli protein

Cited by 25 publications

References 23 publications

MicroRNA-543 inhibits proliferation, invasion and induces apoptosis of glioblastoma cells by directly targeting ADAM9

MicroRNA-543 inhibits proliferation, invasion and induces apoptosis of glioblastoma cells by directly targeting ADAM9

The Role of Wnt Signal in Glioblastoma Development and Progression: A Possible New Pharmacological Target for the Therapy of This Tumor

The Oncogenic Relevance of miR-17-92 Cluster and Its Paralogous miR-106b-25 and miR-106a-363 Clusters in Brain Tumors

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