[Retracted] Long non­coding RNA HOTAIR modulates HLA­G expression by absorbing miR­148a in human cervical cancer.

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].

ELK4 Promotes Cell Cycle Progression and Stem Cell-like Characteristics in HPV-associated Cervical Cancer by Regulating the FBXO22/PTEN Axis

Background: Cervical cancer (CC) is a prevalent gynecological carcinoma, and patients infected with human papillomavirus (HPV) have a higher morbidity rate. Aims: To explore the effects of ETS-like transcription factor 4 (ELK4) in patients with HPV+ CC. Study design: In vitro cell lines and human-sample study. Methods: The ELK4 levels in human tissue (65 HPV+ CC tissue and 25 HPV− normal cervical tissue) and cell lines (human cervical epithelial immortalized cell line H8 and CC cell lines HeLa [HPV18], CaSki [HPV16], and SiHa [HPV−]) were quantified using qRT-PCR and western blot assay. ELK4 knockdown transfection was effective and confirmed by western blotting. The MTT and EDU assays were used to evaluate cell viability and proliferation, respectively. Flow cytometry was used to detect the CC cell cycle stage. Stem cell markers, such as cluster of differentiation 133 (CD133), CD44, and aldehyde dehydrogenase 1, and the cervicospheres formed were measured. ChIP-qPCR and luciferase activity experiments were used to assess the bond between ELK4 and F-box protein 22 (FBXO22). Results: ELK4 was highly expressed in the HPV+ CC tissue. CC cells with ELK4 knockdown had lower viability and proliferation than the control cells. ELK4 knockdown blocked the progression of the cell cycle from G1 to S phase. ELK4 knockdown suppressed the stem cell-like characteristics of the HPV+ CC cells. ELK4 bonded with the FBXO22 promoter, inhibiting the levels of phosphatase and tensin homolog (PTEN). Conclusion: ELK4 facilitated cell cycle progression and stem cell-like characteristics by regulating the FBXO22/PTEN axis. Thus, ELK4 could be a potential therapeutic target to arrest the progress of HPV-associated CC.

Long non-coding RNA HOTAIR modulates HLA-G expression by absorbing miR-148a in human cervical cancer.

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.

miR-182 induces cervical cancer cell apoptosis through inhibiting the expression of DNMT3a.

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.