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Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the HLA western blotting data shown for the HeLa cell line in Fig. 3D on p. 948 were strikingly similar to data appearing in different form in Fig. 3 in the following article written by different authors at different research institutes that was submitted for publication at around the same time, and for which an Expression of Concern has subsequently been published: Sun L, Xue H, Jiang C, Zhou H, Gu L, Liu Y, Xu C and Xu Q: LncRNA DQ786243 contributes to proliferation and metastasis of colorectal cancer both in vitro and in vivo. Biosci Rep 36: e00328, 2016. In addition, it was also noted that certain of the control western blotting data featured in Figs. 3D and 5B were strikingly similar, even though different experiments were being reported on in these figures.  In view of the fact that the contentious data were submitted for publication at around the same time, the Editor of International Journal of Oncology 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. [International Journal of Oncology 49: 943­952, 2016; DOI: 10.3892/ijo.2016.3589].

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Gestational hypertension is one of the complicated disorders during pregnancy; it causes the significant risks, such as placental abruption, neonatal deaths, and maternal deaths. Hypertension is also responsible for the metabolic and cardiovascular issues to the mother after the years of pregnancy. Identifying and treating gestational hypertension during pregnancy by a suitable biomarker is mandatory for the healthy mother and foetus development. Cortisol has been found as a steroid hormone that is secreted by the adrenal gland and plays a pivotal role in gestational hypertension. A normal circulating level of cortisol is involved in the regulation of blood pressure, and it is necessary to monitor the changes in the level of cortisol during pregnancy. In this work, aptamer-based colorimetric assay is demonstrated as a model with gold nanorod to quantify the level of cortisol using the coordinated aggregation (at 500 mM of NaCl) and dispersion (with 10 µM of aptamer), evidenced by the scanning electron microscopy observation and UV-visible spectroscopy analysis. This colorimetric assay is an easier visual detection and reached the limit of detection of cortisol at 0.25 mg/mL. This method is reliable to identify the condition of gestational hypertension during the pregnancy period.

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Insufficient trophoblast migration/invasion is associated with the preeclampsia (PE) development. Recently, microRNAs (miRNAs) have been confirmed to be involved in the pathogenesis of PE. The aim of the present study was to evaluate whether miRNAs is involved in the procession of PE by regulating the migration/invasion of trophoblast. First, we compared the expression profiles of miRNAs between normal and preeclamptic placentas using microarray. Validation analysis of miR-20b level in placentas and peripheral blood specimens was performed using quantitative reverse transcription PCR (qRT-PCR). Then, the effects of miR-20b on trophoblast cell migration and invasion were evaluated using wound healing assay and transwell migration assay. Further bioinformatics analysis, luciferase reporter assays and Western blot were performed to identify its target genes. The correlation between miR-20b and matrix metalloproteinase-2 (MMP-2) in placentas was determined by Pearson's correlation coefficient. Finally, HTR8/SVneo cells were co-transfected with miR-20b inhibitor and si-MMP-2 to explore the molecular mechanism by which miR-20b functions in the trophoblast migration/invasion. We found that miR-20b was elevated in placentas and peripheral blood specimens from preeclampsia patients. Further results show that overexpression of miR-20b significantly inhibited the invasiveness of human trophoblast cells, whereas miR-20b knockdown enhanced trophoblast cell invasion. Matrix metalloproteinase-2 (MMP-2), the most common enzymes in remodeling extracellular matrix components for metastasis, was proved to be a direct target of miR-20b. Inhibition of MMP-2 by siRNA could reverse the promoting effect of miR-20b inhibition on the invasion of trophoblast cells. Taken together, our study indicates that miR-20b inhibited trophoblastic invasion by targeting MMP2. The miR-20b/MMP-2 axis may provide novel insights into understanding the molecular pathogenesis of PE and may be a prognostic biomarker and therapeutic target for PE.

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The long non-coding RNA HOX transcript antisense RNA (HOTAIR) has been found overexpressed in many human malignancies and involved in tumor progression and metastasis. However, little is known about the potential biological roles of HOTAIR in tumor escape. In the present study, the expression of HOTAIR was detected in 59 paired cervical cancer tissue samples by real-time PCR and then subjected to correlation analysis with clinical features. The effects of HOTAIR on cervical cancer cells as well as the expression of human leukocyte antigen (HLA)-G were studied by overexpression and RNA interference approaches. Insight into the mechanism of HOTAIR acting as competitive endogenous RNAs (ceRNAs) was gained from bioinformatic analysis and luciferase assays. HOTAIR expression was obviously increased in cervical cancer tissue. HOTAIR upregulation was associated with advanced pathological stage, histology, lymph node invasion and lymphatic metastasis, and also correlated with shorter overall survival of cervical cancer patients. Furthermore, HOTAIR overexpression promoted the proliferation, migration and invasion of cervical cancer cells, while HOTAIR knockdown inhibited cell invasion and cell viability, induced apoptosis and inhibited growth in vitro and in vivo. Moreover, HOTAIR modulated human leucocyte antigen-G (HLA-G) expression by competitively binding miR-148a. Our data suggest that HOTAIR plays an important oncogenic role in cervical cancer and might serve as a marker for cervical cancer prognosis and a potential target for therapeutic intervention.

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Cervical cancer is the second most common and malignant tumor among women worldwide. However, the effective therapies for this deadly disease are limited because the elaborate molecular mechanism of progress of cervical cancer remains largely unknown. In present study, we not only determine the miR-182 as an anticancer miRNA molecule but also provide the mechanistic link between miR-182 and its anticancer activity. Primarily, the expression of miR-182 is significantly down-regulated in cervical tumor in contrast to normal cervical tissue, and then miR-182 mimic-treated cell presents reduction of cell proliferation and promoting apoptosis. During this process, DNA methyltransferase 3a (DNMT3a) expression is markedly decreased, thereby likely contributing to miR-182-induced apoptosis. Consistently, over-expression of DNMT3a inhibits the miR-182-induced apoptosis, and inhibition of DNMT3a promotes cervical cancer cell apoptosis, which further demonstrated that DNMT3a involved in cervix carcinogenesis. Collectively, we have revealed a valuable mechanism by which down-regulation of DNMT3a contributes to the miR-182-induced cervical cancer cell apoptosis, which raise a becoming potential that miR-182 administration or inhibition of DNMT3a expression may be the underlying strategies for therapeutic intervention in cervical carcinoma.

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