ABSTRACT
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion and migration assay data shown in Figs. 2C and 5D were strikingly similar to data in different form in other articles written by different authors at different research institutes, which had either already been published or had been submitted for publication at around the same time (some of which have now been retracted). Owing to the fact that certain of the data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 36: 23292338, 2016; DOI: 10.3892/or.2016.5007].
ABSTRACT
Glioma is the most frequent primary malignant tumor of the human brain. Recently, great progress has been made in the combined therapy of glioma. However, the clinical effects of these treatments and prognosis for patients with glioma remains poor. MicroRNAs (miRNAs) have been demonstrated to play important roles in the initiation and progression of various types of human cancers, also including glioma. The present study investigated the expression patterns of microRNA140 (miR-140) in glioma, and the roles of miR-140 in glioma cell proliferation, migration and invasion. The results showed that miR-140 was significantly downreuglated in glioma tissues and cell lines, and low expression levels of miR-140 were correlated with World Health Organization (WHO) grade and Karnofsky performance score (KPS) of glioma patients. Restoration of miR-140 obviously suppressed glioma cell proliferation, migration and invasion. In addition, a disintegrin and metalloproteinase 9 (ADAM9) was identified as a novel direct target gene of miR-140 in glioma. Furthermore, knockdown of ADAM9 simulated the tumor suppressor functions of miR-140, while overexpression of ADAM9 abrogated these suppressive effects induced by miR-140 in glioma cells. In conclusion, the present study demonstrated the expression and clinical roles of miR-140 in glioma and suggested that miR-140 inhibited proliferation, migration and invasion of glioma cells, partially at least via suppressing ADAM9 expression. Therefore, miR-140 may be a novel candidate target for the development of therapeutic strategies for patients with glioma.
Subject(s)
ADAM Proteins/genetics , Cell Proliferation/genetics , Glioma/genetics , Membrane Proteins/genetics , MicroRNAs/genetics , ADAM Proteins/biosynthesis , Adult , Aged , Cell Line, Tumor , Cell Movement/genetics , Female , Gene Expression Regulation, Neoplastic , Glioma/pathology , Humans , Karnofsky Performance Status , Male , Membrane Proteins/biosynthesis , MicroRNAs/biosynthesis , Middle Aged , Neoplasm Invasiveness/genetics , Neoplasm Metastasis , PrognosisABSTRACT
OBJECTIVE: To construct the recombinant adenovirus vector expressing human endostatin. METHODS: Human endostatin gene extracted from pGEM-T Easy vector containing the target gene fragment was successfully amplified using PCR and cloned into pShuttle2 vector. The target gene was subcloned into an adenovirus vector and the resulted recombinant adenovirus (Ad-hEndo) was linearized before transfected into HEK 293 packaging cells. The Ad-hEndo recombinant adenovirus was efficiently amplified in 293T cells and purified by CsCl density centrifugation, and the titer of the virus was determined. RESULTS: The amplified hEndostatin cDNA was verified by PCR and sequencing, and the resulted virus titer reached 5.2 x 10(9) pfu/ml. CONCLUSION: The recombinant adenovirus containing human endostatin gene has been successfully constructed, which may provide important basis for gene therapy research for angiogenesis-dependent diseases.