[Retracted] Role of the AKT pathway in microRNA expression of human U251 glioblastoma cells.

Following the publication of the above article, a concerned reader drew to the Editor's attention that, regarding the western blots featured in Fig. 3B on p. 670, the bands featured in the U251 and U251‑MC lanes for the miR‑21 and U6 experiments appeared to be duplicates of each other.

MUC1 promotes glioblastoma progression and TMZ resistance by stabilizing EGFRvIII.

Epidermal growth factor receptor variant III (EGFRvIII) is a mutant isoform of EGFR with a deletion of exons 2-7 making it insensitive to EGF stimulation and downstream signal constitutive activation. However, the mechanism underlying the stability of EGFRvIII remains unclear. Based on CRISPR-Cas9 library screening, we found that mucin1 (MUC1) is essential for EGFRvIII glioma cell survival and temozolomide (TMZ) resistance.

MiR-221 and miR-222 target PUMA to induce cell survival in glioblastoma.

Background: MiR-221 and miR-222 (miR-221/222) are frequently up-regulated in various types of human malignancy including glioblastoma. Recent studies have reported that miR-221/222 regulate cell growth and cell cycle progression by targeting p27 and p57. However the underlying mechanism involved in cell survival modulation of miR-221/222 remains elusive.

MicroRNA-221 and microRNA-222 regulate gastric carcinoma cell proliferation and radioresistance by targeting PTEN.

Background: MicroRNAs (miRNAs) can function as either oncogenes or tumor suppressor genes via regulation of cell proliferation and/or apoptosis. MiR-221 and miR-222 were discovered to induce cell growth and cell cycle progression via direct targeting of p27 and p57 in various human malignancies. However, the roles of miR-221 and miR-222 have not been reported in human gastric cancer.

Downregulation of Dicer enhances tumor cell proliferation and invasion.

miRNAs are non-coding, single-stranded RNAs that regulate target gene expression by repressing translation or promoting RNA cleavage. Dicer is an essential component of the miRNA processing machinery. To identify a role for miRNAs in tumorigenesis, we designed an adenovirus expressing small hairpin RNA (shRNA) to silence Dicer and globally suppress the maturation of miRNAs.

Co-delivery of as-miR-21 and 5-FU by poly(amidoamine) dendrimer attenuates human glioma cell growth in vitro.

MicroRNAs have been demonstrated to be deregulated in different types of cancer. miR-21 is a key player in the majority of cancers. Down-regulation of miR-21 in glioblastoma cells leads to repression of cell growth, increased cellular apoptosis and cell-cycle arrest, which can theoretically enhance the chemotherapeutic effect in cancer therapy.

Role of the AKT pathway in microRNA expression of human U251 glioblastoma cells.

Activation of the AKT (serine-threonine kinase) pathway is a common feature in glioblastoma cells. Downstream factors of the AKT pathway are involved in cell proliferation, apoptosis, cellular migration and angiogenesis. Micro-RNAs (miRNAs) are highly conserved small non-coding RNAs that block targeted mRNA expression at the post-transcriptional level.

MicroRNA-21 inhibitor sensitizes human glioblastoma cells U251 (PTEN-mutant) and LN229 (PTEN-wild type) to taxol.

Background: Substantial data indicate that the oncogene microRNA 21 (miR-21) is significantly elevated in glioblastoma multiforme (GBM) and regulates multiple genes associated with cancer cell proliferation, apoptosis, and invasiveness. Thus, miR-21 can theoretically become a target to enhance the chemotherapeutic effect in cancer therapy. So far, the effect of downregulating miR-21 to enhance the chemotherapeutic effect to taxol has not been studied in human GBM.

Downregulation of miR-21 enhances chemotherapeutic effect of taxol in breast carcinoma cells.

The successful of anti-cancer treatment are often limited by the development of drug resistance. Recent work has highlighted the involvement of non-coding RNAs, microRNAs(miRNAs) in cancer development, and their possible involvement in the evolution of drug resistance has been proposed. In this study, we combine taxol chemotherapy and miR-21 inhibitor treatment via polyamidoamine (PAMAM) dendrimers vector to evaluate the effects of combination therapy on suppression of breast cancer cells.

Overexpression of septin 7 suppresses glioma cell growth.

Our previous study demonstrated that SEPT7 was downregulated at mRNA level in human gliomas. This study is to further examine the expression of SEPT7 in glioma samples and characterizes its role on cell cycle progression and growth of glioma cells. mRNA and protein expression of SEPT7 were detected by RT-PCR, immunohistochemical staining, and western blot analysis in human glioma specimens and normal brain tissues.

[Inhibitory effect of knocking down microRNA-221 and microRNA-222 on glioma cell growth in vitro and in vivo].

Objective: To study the inhibitory effect of knocking down microRNA(miR)-221 and miR-222 on human glioma cell growth and its possible mechanism.

Methods: miRNA-221/222 antisense oligonucleotides (antisense miR221/222) were transfected into human glioma U251 cells by lipofectamine. Northern blot analysis was conducted to detect the mRNA expression of miR-221/222 in the control and transfected cell groups.

[The effect of silencing Dicer by small interference RNA on the biological characteristics of human glioma cells].

Objective: To study the effect of silencing Dicer by small interference RNA (siRNA) to suppress the global microRNA (miRNAs) expression on the biological characteristics of TJ905 glioblastoma cells.

Methods: The silencing effect of RNA interference on Dicer expression was evaluated by reverse transcription-polymerase chain reaction (RT-PCR), Western blot analysis and immunofluorescence staining. The cell proliferation rate and cell cycle kinetics were detected by MTT assay and flow cytometry respectively, and the cell invasive ability was evaluated by transwell assay.

Combination gene therapy with PTEN and EGFR siRNA suppresses U251 malignant glioma cell growth in vitro and in vivo.

The over-expression/amplification of the epidermal growth factor receptor (EGFR) gene and mutation/deletion of tumor suppressor PTEN gene are main genetic changes identified in glioblastomas. These two genetic changes play a critical role in the formation of many malignant tumors and have been shown to be the important therapeutic targets. In this study, we used an expression plasmid that expresses small hairpin RNA-targeting sequences of human EGFR and wild-type PTEN cDNA to examine the growth inhibitive effects in U251 glioma cells.

[Differential expression of Notch1 and Notch2 in astrocytoma and medulloblastoma].

Objective: To detect the differential expression of Notch1 and Notch2 in human astrocytoma and medulloblastoma; and to study the role of Notch1 and Notch2 in the development of both tumors.

Methods: Immunohistochemical staining (SP method) and Western blot analysis were used to detect Notch1 and Notch2 expression in tissue arrays and freshly resected samples of normal brain tissue, astrocytoma and medulloblastoma.

Results: Notch1 and Notch2 were negative in normal human brain tissue.

[Study on the anti-invasion effect of SEPT7 gene for U251MG glioma cell in vitro].

Objective: To study the anti-invasion effect of SEPT7 gene on U251MG glioma cells and its possible molecular mechanism.

Methods: Recombinant adenovirus vector carrying SEPT7 gene (rAd5-SEPT7) was transduced to human glioma cell line U251MG, and empty adenovirus vector was used as control. Tumor invasion was examined by Transwell method and 3 D-Matrigel assay, and tumor cell migration by wound-healing method and 2 D-Matrigel assay.

[Influence of SEPT7 on biological characters of glioma cell line TJ905].

Objective: To investigate the influence of SEPT7 on biological characters of gliomas cells TJ905.

Methods: Recombinant SEPT7 constructs was transfected to human glioblastoma cell line TJ905 in which SEPT7 expression is absent. The positive clones were identified by RT-PCR and Western blot analysis.

[Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway].

Objective: To study further the most important and frequent genetic alterations of p53 and epidermal growth factor receptor (EGFR) in astrocytic gliomas.

Methods: (1) EGFR expression was examined in samples collected from 37 astrocytic gliomas and 6 normal brain tissue using reverse transcriptase polymerase chain reaction and immunohistochemical staining. (2) p53 gene mutation and accumulation were detected simultaneously in the same specimens using PCR-SSCP, DNA sequencing and immunohistochemical staining.

An in vitro study on the suppressive effect of glioma cell growth induced by plasmid-based small interference RNA (siRNA) targeting human epidermal growth factor receptor.

Objectives: To study the inhibitory effects of plasmid-based siRNA targeting human epidermal growth factor receptor (EGFR) on tumor proliferation and invasion of TJ905 glioblastoma cells.

Methods: Two siRNA expression constructs targeting human EGFR extracellular domain (516-536) and catalytic domain (2400-2420) were transfected into TJ905 cell as mediated by Lipofectamine. Immunofluorescence assay and Western blotting were used to detect EGFR expression.

[Inhibitory effect of antisense and dominant-negative AKT2 constructs on proliferation of glioma cell line TJ905].

Background & Objective: Serine/threonine kinase (AKT) mediates a downstream signal transduction pathway of epidermal growth factor receptor (EGFR), and plays an important role in survival and apoptosis of tumor cells. This study was designed to investigate regulation of antisense AKT2 (AS-AKT2) and dominant-negative AKT2 (DN-AKT2) constructs on proliferation and apoptosis of glioma cell line TJ905.

Methods: AS-AKT2 and DN-AKT2 were transfected into TJ905 cells, 3 stably transfected clones were randomly selected from each group, and amplified for further study.

[Inhibitory effects of siRNA targeting epidermal growth factor receptor on proliferation and invasion of human glioblastoma cells].

Objective: To study the inhibitory effects of siRNA targeting epidermal growth factor receptor (EGFR) on the proliferation and invasion of human glioblastoma cells.

Method: Two siRNA expression constructs using psiRNA-NeoG2 vector, that targeted sequences of human EGFR receptor L domain (516 - 536) and catalytic domain (2400 - 2420) respectively, were constructed. Human malignant glioma cells of the line TJ905 were cultured in vitro and transfected with pcDNA3-hEGFR, anti-sense RNA, blank vector psiRNA-NeoG2 (as negative control), psiRNA-NeoG2-516, and psiRNA-NeoG2-2400 respectively mediated by LipofectAMINE.

[Preliminary study on the gene expression profiles of ependymomas with cDNA array].

Objective: To investigate the differential gene expression of ependymomas.

Methods: Four fresh samples of ependymomas and 1 of normal brain tissue were collected during operation. The extracted total RNAs were converted as (32)P tagged cDNA probes, which were then hybridized with the Atlas Human Cancer Array, producing the array based hybridization maps following the protocol provided with the kit.

[Preliminary study on the mechanism of connexin 43 gene transfection in the control of glioma cell proliferation].

Objective: To study the mechanism involved in the control of glioma cell proliferation with transfection of connexin (Cx) 43 gene.

Methods: C6 rat glioma and TJ905 human glioblastoma cell lines without Cx43 gene expression were transfected with Cx43cDNA mediated by lipofectamine. Northern blot, in situ hybridization and immunohistochemical technology were used to detect the expression of Cx43mRNA and its protein with MTT assay and silver colloid stain for the detection of cell proliferation, TUNEL method for determination of cell apoptosis, scrape loading dye transfer (SLDT) for GJIC, Western blot and immunohistochemical technology for bFGF, PDGF, EGFR, IGF-I and IGFBP3 expression.