Knockdown of ILK inhibits glioma development via upregulation of E-cadherin and downregulation of cyclin D1

Zheng, Kewen; Wang, Guangyi; Li, Chunhui; Shan, Xiaosong; Liu, Haipeng

doi:10.3892/or.2015.3983

Cited by 8 publications

(9 citation statements)

References 20 publications

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“…Taken together, these data suggest that mir-218-2 modulates the APC/Cubiquitin–proteasome pathway by targeting CDC27 in glioma cells. Moreover, taking into account that adhesion and cell junction proteins, such as E-cadherin [23, 24], β-catenin [25], focal adhesion kinase (FAK)[26], and vinculin [27] play important roles in cell migration and invasion, we determined their levels of expression by performing Western blotting (Figure 5F–5I). The expression of E-cadherin, in contrast to βcatenin, was decreased in the mir-218-2 group compared to the CGs.…”

Section: Resultsmentioning

confidence: 99%

“…Importantly, CDC27 has been associated with securin expression and serve as an inverse predictor for the presence of malignant cells and shortened survival in human breast tumor cases [34]. In contrast, cyclin proteins, such as cyclin A [35], cyclin B [36] and cyclin D1 [24, 37, 38], express aberrantly in tumor species. The cyclin/CDK, cyclin A/CDK2, and cyclin D/CDK4 complexes play critical roles in cell cycle control and DNA replication.…”

Section: Discussionmentioning

confidence: 99%

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mir-218-2 promotes glioblastomas growth, invasion and drug resistance by targeting CDC27

et al. 2016

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Glioma has become a significant global health problem with substantial morbidity and mortality, underscoring the importance of elucidating its underlying molecular mechanisms. Recent studies have identified mir-218 as an anti-oncogene; however, the specific functions of mir-218-1 and mir-218-2 remain unknown, especially the latter. The objective of this study was to further investigate the role of mir-218-2 in glioma. Our results indicated that mir-218-2 is highly overexpressed in glioma. Furthermore, we showed that mir-218-2 is positively correlated with the growth, invasion, migration, and drug susceptibility (to β-lapachone) of glioma cells. In vitro, the overexpression of mir-218-2 promoted glioma cell proliferation, invasion, and migration. In addition, the overexpression of mir-218-2 in vivo was found to increase glioma tumor growth. Accordingly, the inhibition of mir-218-2 resulted in the opposite effects. Cell division cycle 27 (CDC27), the downstream target of mir-218-2, is involved in the regulation of glioma cells. Our results indicate that the overexpression of CDC27 counteracted the function of mir-218-2 in glioma cells. These novel findings provide new insight in the application of mir-218-2 as a potential glioma treatment.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mir-218-2 promotes glioblastomas growth, invasion and drug resistance by targeting CDC27

et al. 2016

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“…Integrin signalling through ILK has been reported to upregulate the transcriptional repressors SNAIL/SLUG and subsequently suppress E-cadherin transcription 23 – 25 . Accordingly, our results indicated that the decrease in integrin-β1 led to reduced ILK expression, and subsequently contributed to the upregulation and downregulation of the EMT-related molecules E-cadherin and Snail, respectively.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia-inducible ERO1α promotes cancer progression through modulation of integrin-β1 modification and signalling in HCT116 colorectal cancer cells

Takei

Yoneda

Sakai-Sawada

et al. 2017

Sci Rep

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Endoplasmic reticulum disulphide oxidase 1α (ERO1α) is an oxidase localized in the endoplasmic reticulum that plays a role in the formation of disulphide bonds of secreted and cell-surface proteins. We previously showed that ERO1α is overexpressed in various types of cancer and we further identified ERO1α expression as a novel factor related to poor prognosis in cancer. However, the biological functions of ERO1α in cancer remain unclear. Here, we investigated the cell biological roles of ERO1α in the human colon-cancer cell line HCT116. ERO1α knockout (KO) by using CRISPR/Cas9 resulted in decreased tumourigenicity in vivo and reduced cell proliferation only under hypoxia in vitro, which suggested that ERO1α promotes cancer progression specifically in a low-oxygen environment. Thus, we evaluated the function of ERO1α in cell proliferation under hypoxia, and found that under hypoxic conditions, ERO1α KO resulted in a contact-inhibited morphology and diminished motility of cells. We further showed that ERO1α KO induced a change in integrin-β1 glycosylation and thus an attenuation of cell-surface integrin-β1 expression, which resulted in the aforementioned phenotype. Our study has established a previously unrecognized link between ERO1α expression and integrin activation, and thus provides new evidence for the effectiveness of ERO1α-targeted therapy for colorectal carcinoma.

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“…Knock-down of RRM2 also significantly elevated the expression of E-cadherin ( Fig. 3E-3F), a suppressor of glioma development and invasion [43]. Additionally, more apoptotic cells were detected by flow cytometry in the shRRM2-transfected cells than the negative control, accompanied by upregulation of cleaved caspase-3 and downregulation of BCL-2 ( Fig.…”

Section: Discussionmentioning

confidence: 81%

RRM2 is a potential prognostic biomarker with functional significance in glioma

Sun¹,

Yang²,

Zhang³

et al. 2019

Int. J. Biol. Sci.

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Glioma is one of the most common brain tumors, suggesting the importance of investigating the molecular mechanism of gliomas. We studied the roles of Ribonucleotide Reductase Regulatory Subunit M2 (RRM2) in glioma. Expressions of RRM2 are higher in glioma tissues evidenced by TCGA data, western blot and immunohistochemistry. RRM2 is negatively correlated with glioma patient's survival. RNA-seq showed that genes involved in apoptosis, proliferation, cell adhesion and negative regulation of signaling were up-regulated upon RNAi-mediated knock-down of RRM2. Cell phenotypes specific for stably knocking down RRM2 were determined using stable transfection in vitro. In an in vivo model, knock-down of RRM2 inhibited tumor growth and caused suppression of AKT and ERK1/2 signalings. Interfering RRM2 also down-regulated the expression of cyclin A, cyclin B1, cyclin D1, Vimentin, and N-cadherin, and elevated E-cadherin expression. Moreover, overexpression of RRM2 failed to increase the expression of cyclin B1, cyclin D1, and N-cadherin when phosphorylation of AKT and ERK1/2 was suppressed by LY294002 or PD98059. These findings indicated that RRM2 is a positive regulator of glioma progression which contributes to the migration and proliferation of glioma cells through ERK1/2 and AKT signalings and might be a novel prognostic indicator for glioma patients.

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Knockdown of ILK inhibits glioma development via upregulation of E-cadherin and downregulation of cyclin D1

Cited by 8 publications

References 20 publications

mir-218-2 promotes glioblastomas growth, invasion and drug resistance by targeting CDC27

mir-218-2 promotes glioblastomas growth, invasion and drug resistance by targeting CDC27

Hypoxia-inducible ERO1α promotes cancer progression through modulation of integrin-β1 modification and signalling in HCT116 colorectal cancer cells

RRM2 is a potential prognostic biomarker with functional significance in glioma

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