[Retracted] miRNA­1207­5p is associated with cancer progression by targeting stomatin­like protein 2 in esophageal carcinoma.

Subsequently to the publication of the above article, and a Corrigendum that has already been published with the intention of showing corrected versions of Figs. 3 and 6 (DOI: 10.3892/ijo.2018.4254; published online on January 24, 2018), a concerned reader drew to the Editor's attention that there appeared to be an unexpected overlap of data in a couple of the panels showing flow cytometric data in Fig. 3A; furthermore, strikingly similar data also appeared in a paper that was submitted to the journal Cancer Gene Therapy at around the same time [Zang W, Wang T, Huang J, Li M, Wang Y, Du Y, Chen X and Zhao G: Long noncoding RNA PEG10 regulates proliferation and invasion of esophageal cancer cells. Cancer Gene Ther 22: 138­144, 2015]. Considering the latest discrepancies and concerns that have been raised with another of the figures in this paper, the Editor of International Journal of Oncology has decided that the article should be retracted from the publication. 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 of the Journal for any inconvenience caused. [International Journal of Oncology 46: 2163­2171, 2015; DOI: 10.3892/ijo.2015.2900].

Retraction Note: Mir-655 up-regulation suppresses cell invasion by targeting pituitary tumor-transforming gene-1 in esophageal squamous cell carcinoma.

The Editor-in-Chief has retracted this article [1] because Figure 3a overlaps with Figure 2 in [2]. An investigation by Zhengzhou University has confirmed this. The data reported in this article are therefore unreliable. There is also considerable text overlap with a previously published article [3]. Guoqiang Zhao does not agree with this retraction. The other authors have not responded to correspondence from the editor about this retraction.

Knockdown of lncRNAXLOC_001659 inhibits proliferation and invasion of esophageal squamous cell carcinoma cells.

BACKGROUND: Studies have shown that long non-coding RNAs (lncRNAs) play a key role in almost all key physiological and pathological processes, including different types of malignant tumors. Our previous lncRNA microarray results have shown that lncRNA XLOC_001659 is upregulated in esophageal cancer (EC) tissues, with a fold change of 20.9 relative to normal esophageal tissues. But its effect and the molecular biological mechanisms on proliferation and invasion of EC cells remain unclear. AIM: To investigate the effect of lncRNA XLOC_001659 on esophageal squamous cell carcinoma (ESCC) cells and explore the molecular biological mechanisms involved. METHODS: RT-qPCR assay was used to quantify the expression levels of lncRNAXLOC-001659 and miR-490-5p. The proliferative capacity of the cells was determined using CCK8 and colony formation assays, and the effect of lncRNAXLOC-001659 on the invasion of ESCC cells was determined by Transwell assay. Dual-luciferase reporter assay was used to detect the target genes of lncRNAXLOC-001659 and miR-490-5p. RESULTS: The results of RT-qPCR showed that the expression of lncRNAXLOC_001659 was upregulated in ESCC cells. CCK-8 assay showed that knockdown of lncRNAXLOC_001659 significantly inhibited ESCC cell proliferation. Colony formation and Transwell invasion assays showed that knockdown of lncRNAXLOC_001659 or overexpression of miR-490-5p significantly inhibited ESCC cell growth and invasion. Furthermore, lncRNAXLOC_001659 acts as an endogenous sponge by competitively binding to miR-490-5p to downregulate miR-490-5p. Further results confirmed that miR-490-5p targeted PIK3CA, and the recovery of PIK3CA rescued lncRNAXLOC_001659 knockdown or miR-490-5p overexpression-mediated inhibition of cell proliferation and invasion, which suggested the presence of an lncRNAXLOC_001659/miR-490-5p/PIK3CA regulatory axis. CONCLUSION: Knockdown of lncRNA XLOC_001659 inhibits proliferation and invasion of ESCC cells via regulation of miR-490-5p/PIK3CA, suggesting that it may play a role in ESCC tumorigenesis and progression.

Retraction Note to: Effect of miR-451 on the Biological Behavior of the Esophageal Carcinoma Cell Line EC9706.

The Editor-in-Chief has retracted this article [1] because Figure 8 overlaps with Figure 6b of [2] and Figure 6 overlaps with Figure 3 of [3] and Figure 3 of [4].

Retraction Note: miR-663 attenuates tumor growth and invasiveness by targeting eEF1A2 in pancreatic cancer.

The Editor-in-Chief has retracted this article [1] because Figure 6b overlaps with Figure 8 of [2] and Figure 4a overlaps with Figure 2b of [3].

Retraction Note: Overexpression of A613T and G462T variants of DNA polymerase ß weakens chemotherapy sensitivity in esophageal cancer cell lines.

[This retracts the article DOI: 10.1186/s12935-016-0362-x.].

MiR-149 sensitizes esophageal cancer cell lines to cisplatin by targeting DNA polymerase ß.

Human DNA polymerase ß (polß) is a small, monomeric protein essential for short-patch base excision repair (BER). polß plays an important role in the regulation of chemotherapy sensitivity in tumour cells. In this study, we determined that the expression levels of polß mRNA and miR-149 in tumour tissues were significantly higher than in adjacent non-tumour tissues. We also found that the expression level of miR-149 in EC tumour tissues was inverse to that of polß expression. Bioinformatics analysis and dual-luciferase reporter assay predicted that miR-149 negatively regulates polß expression by directly binding to its 3'UTR. CCK-8 assay indicated that miR-149 could enhance the anti-proliferative effects of cisplatin in EC1 and EC9706 cell lines. Flow cytometry, caspase 3/7 activity, and immunofluorescence microscopy results indicated that miR-149 could enhance the apoptotic effects of cisplatin in EC1 and EC9706 cell lines. We also showed that the expression of polß lacking the 3'UTR sequence could override the proliferative and apoptotic functions of miR-149, suggesting that miR-149 negatively regulates polß expression by binding to its 3'UTR. Surface plasmon resonance results also showed that miR-149 could bind with wild-type polß. In addition, we identified a new variant of polß (C1134G). In conclusion, this study confirms that miR-149 may enhance the sensitivity of EC cell lines to cisplatin by targeting polß, and that miR-149 may be unable to regulate the C1134G variant of polß. Based on these findings, potential drugs could be developed with a focus on enhanced sensitivity of EC patients to chemotherapy.

[Corrigendum] miRNA-1207-5p is associated with cancer progression by targeting stomatin-like protein 2 in esophageal carcinoma.

An interested reader drew to our attention that, in the above-mentioned article, there were two figures where identity in certain of the data was shared between panels within the same figure. First, in Fig. 3B, the data shown for the EC9706 cell line/negative control (NC) experiment were derived from the same original source as those for the EC-1/Blank control experiment. Secondly, in Fig. 6B the Bcl-2 bands for the two different cell lines, EC9706 and EC-1, were inadvertently duplicated (the data shown for the EC9706 cell line were correct). We have reviewed the original files and the individual figures for the submitted composite figures, and realize that the errors occurred when we produced the composite figures. The same images were accidentally inserted twice in Figs. 3 and 6 without us being fully aware of the error. We have identified all the original images, and the corrected versions of Figs. 3 and 6 are shown opposite. We regret that these errors went unnoticed prior to publication, and thank the Editor for affording us the opportunity to publish this Corrigendum. We also regret any inconvenience caused to the readership of the journal. [the original article was published in the International Journal of Oncology 46: 2163-2171, 2015; DOI: 10.3892/ijo.2015.2900].

[Retracted] Effects of cyclin E gene silencing on the proliferation of esophageal cancer cell lines, EC9706, Eca109 and KYSE30.

Subsequently to the publication of this article, an interested reader drew to our attention the fact that the six panels shown in Fig. 6 shared several areas of identity among them. Following an internal investigation, a laboratory technician, who was responsible for editing the pictures, admitted that the data as presented in the figure had been manipulated after having mislaid some of the original data. The corresponding author of the article takes responsibility for this oversight, and therefore the paper is to be retracted from publication. All of the named authors agree to this retraction. We deeply regret that these errors were allowed to remain in the paper, and extend our apologies to the readership of the Journal. [the original article was published in Molecular Medicine Reports 7: 799-804, 2013; DOI: 10.3892/mmr.2013.1280].

α-solanine enhances the chemosensitivity of esophageal cancer cells by inducing microRNA­138 expression.

Esophageal cancer is a common malignant tumor worldwide. Inherent and acquired drug resistance are the major challenges faced in anticancer chemotherapy. This study aimed to explore the effects of α-solanine in regards to the chemosensitivity of esophageal cancer cells. We found that α-solanine enhanced the sensitivity of EC9706 and KYSE30 cells to 5-flurouracil (5-FU) and cisplatin (Cis) by promoting drug-induced apoptosis. qRT-PCR and western blotting results showed that α-solanine treatment promoted miR-138 expression and decreased survivin expression in EC9706 and KYSE30 cells. α-solanine also enhanced the inhibitory effects of 5-Fu and Cis in EC9706 transplanted tumors in mouse models. Dual-Luciferase reporter assay results confirmed survivin as the direct target gene of miR-138. MiR-138 inhibited survivin expression in EC9706 and KYSE30 cells. And miR-138 mimic and si-survivin had similar effects with α-solanine in suppressing survivin expression and promoting cancer cell death. miR-138 inhibitor reversed the chemosensitivity-enhancing effect of α-solanine. In EC9706 and KYSE30 cells, survivin overexpression rescued the cancer cells from apoptosis caused by α-solanine and miR-138 mimic expression. From these findings, we conclude that α-solanine enhanced the chemosensitivity of esophageal cancer cells to chemotherapy via the miR-138/survivin pathway. This study provides insight into the molecular mechanism underlying the chemosensitivity-enhancing function of α-solanine and suggests a new chemotherapeutic strategy for esophageal cancer treatment.

RETRACTED: The long noncoding RNA CASC2 inhibits tumorigenesis through modulating the expression of PTEN by targeting miR-18a-5p in esophageal carcinoma.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. In the article Figure 3A top and center panel are duplicated and in Figure 5A elements are duplicated from previous publications from the same authors in Tumor Biol. (2014) 35:12583­12592 DOI 10.1007/s13277-014-2579-4 (Figure 3) and Dig Dis Sci (2013) 58:706­714 DOI 10.1007/s10620-012-2395-x (Figure 8). The authors recognize mishandling of these images which affects the validation of the study and would like to apologize to readers.

Overexpression of A613T and G462T variants of DNA polymerase ß weakens chemotherapy sensitivity in esophageal cancer cell lines.

BACKGROUND: Human DNA polymerase ß (polß) is a small monomeric protein that is essential for short-patch base excision repair. It plays an important role in regulating the sensitivity of tumor cells to chemotherapy. METHODS: We evaluated the mutation of polß in a larger cohort of esophageal cancer (EC) patients by RT-PCR and sequencing analysis. The function of the mutation was evaluated by CCK-8, in vivo tumor growth, and flow cytometry assays. RESULTS: There are 229 patients with the polß mutation, 18 patients with A613T mutation, 12 patients with G462T mutation among 538 ECs. Analysis results of survival time showed that EC patients with A613T, G462T mutation had a shorter survival than the others (P < 0.05). CCK-8 and flow cytometry assays results showed the A613T, G462T EC9706 cells were less sensitive than WT cells to 5-FU and cisplatin (P < 0.05). Experiments results in vivo showed that the tumor sizes of A613T and G462T group were larger than WT and polß-/- groups (P < 0.05). CONCLUSIONS: In this study, we discovered A to T point mutation at nucleotide 613 (A613T) and G to T point mutation at nucleotide 462 (G462T) in the polß gene through 538 EC patients cohort study. A613T and G462T variant of DNA polymerase ß weaken chemotherapy sensitivity of esophageal cancer.

Inhibitory effect of α-solanine on esophageal carcinoma in vitro.

α-solanine, a bioactive component and one of the major steroidal glycoalkaloids in potatoes, has been observed to inhibit growth and induce apoptosis in cancer cells. However, the antitumor efficacy of α-solanine on esophageal carcinoma has yet to be fully elucidated. In the present study, the antitumor efficacy of α-solanine against human esophageal carcinoma cells was investigated. It was determined that α-solanine inhibited the growth and proliferation of human esophageal EC9706 and Eca109 cancer cells in a dose-dependent manner, as well as the cell migration and invasion. In addition, the apoptotic rate was increased in the cancer cells treated with α-solanine in a dose-dependent manner, compared with that of the control group (P<0.05). The expression levels of tumor metastasis-related proteins, including matrix metalloproteinase (MMP)-2 and MMP-9, were reduced in the cells treated with α-solanine, as compared with the control group. Conversely, significantly higher expression levels of E-cadherin were detected in the α-solanine-treated groups, as compared with the control group (P<0.05). Therefore, the current results provide a novel insight into the anti-tumor mechanism of α-solanine, and suggest that α-solanine is a potential agent for the prevention and treatment of esophageal carcinoma.

α-Solanine Modulates the Radiosensitivity of Esophageal Cancer Cells by Inducing MicroRNA 138 Expression.

BACKGROUND: Esophageal cancer (EC) is one of the most common malignant tumors in the world. Due to difficulties with performing the operation, most patients choose to have palliative treatment instead. Radiotherapy is one of the main palliative treatments of EC. However, the clinical efficacy of radiotherapy is not satisfactory α-Solanine is a bioactive component of steroidal glycoalkaloids which has been demonstrated to exhibit anti-metastasis activity in different cancers. In the present study, we determined the effect of α-solanine on the radiosensitivity of EC cells and priliminarily explored the underlying molecular mechanisms. METHODS: Cell Counting Kit-8 (CCK-8) assay was conducted to found the cytotoxic effect of α-solanine on EC cells. CCK-8 assay and colony-forming survival assays were performed to explore the effect of α-solanine on cell viability and proliferation of EC cells after irradiation. Immunofluorescence and comet assays were used to detect the effect of α-solanine on DNA repair capacity of EC cells after irradiation. The flow cytometry (FCM) and Hoechst/PI staining were conductd to study the effect of α-solanine on apoptosis of EC cells after irradiation. RESULTS: The cytotoxic effect of α-solanine to EC cells was dose-dependent. The results of CCK-8, colony-forming survival assay, immunofluorescence, comet assay, FCM and Hoechst/PI staining showed that α-solanine could enhance the radiosensitivity of EC cells. α-Solanine could downregulate Survivin expression level by upregulating miR-138 expression in EC cells. Upregulation of miR-138 and knock down Survivin both enhanced the radiosensitivity of EC cells. Moreover, Survivin could restore the effect of α-solanine and miR-138 on radiosensitivity of EC cells. CONCLUSIONS: α-solanine could enhance the radiosensitivity of esophageal cancer cells by inducing microRNA-138 expression, and probably be an effective radiosensitizer in treating EC.

Curcumin inhibits cell growth and induces cell apoptosis through upregulation of miR-33b in gastric cancer.

In this work, the in vitro experiments about biological mechanisms of curcumin were conducted using the gastric cancer cell lines SGC-7901 and BGC-823. After 24-h exposure to curcumin at the concentrations of 5, 10, 15, 20, and 40 µmol/L, two cells showed the decreased proliferation and increased apoptosis abilities. Real-time PCR, Cell Counting Kit-8 (CCK-8) assay, western blotting, and cell apoptosis assay were used to further study the underlying mechanisms of curcumin. The first stage of our studies showed that curcumin affected the expression of miR-33b, which, in turn, affected the expression of the X-linked inhibitor of apoptosis protein (XIAP) messenger RNA (mRNA). Next, curcumin was also identified to regulate the proliferation and apoptosis of SGC-7901 and BGC-823 cells. Further bioinformatics analysis and luciferase reporter assays proved that XIAP was one of the target genes of miR-33b. In the next stage, SGC-7901 and BGC-823 cells were treated with 20 µL curcumin, miR-33b mimics, and small interfering RNA (siRNA) of XIAP, respectively. The results showed that curcumin had similar effects on cell growth and apoptosis as the upregulation of miR-33b and the upregulation of the siRNA of XIAP. The results that followed from the restore experiments showed that curcumin affected cell growth and apoptosis presumably by upregulating the XIAP targeting in gastric cancer. Collectively, our results indicate that curcumin-miR-33b-XIAP coupling might be an important mechanism by which curcumin induces the apoptosis of SGC-7901 and BGC-823 cells.

LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma.

Recently, the incidence of melanoma has been on the rise. Patients with distant metastasis share poor prognosis. Increasing studies have been conducted to clarify the molecular mechanisms as well as to investigate potential effective therapeutic targets in the development of melanoma. This study focuses on the LncRNA UCA1 and its downstream regulated factors. In our experiments, UCA1 expression was discovered to be upregulated in melanoma tissues and cells, while the depletion of UCA1 led to the inhibition of cell proliferation, invasion and cell cycle arrest. To further our understanding of the mechanisms of UCA1, a system of experiments was built. We found that miR-507 could directly bind to UCA1 at the miRNA recognition site, and that there was a negative correlation between miR-507 and UCA1. Additionally, FOXM1 is a target of miR-507 and can be downregulated by either miR-507 overexpression or UCA1 depletion. Downregulated FOXM1 was analogous to the depletion of UCA1 and the overexpression of miR-507. These results, taken together, provide evidence for a novel UCA1 interaction regulatory network in tumorigenesis of melanoma.

Knockdown of long non-coding RNA TP73-AS1 inhibits cell proliferation and induces apoptosis in esophageal squamous cell carcinoma.

Recent studies have shown that long non-coding RNAs (lncRNAs) are involved in a variety of biological processes and diseases in humans, including cancer. Our study serves as the first comprehensive analysis of lncRNA TP73-AS1 in esophageal cancer. We utilized a lncRNA microarray to analyze the expression profile of lncRNAs in esophageal squamous cell carcinoma. Our results show that lncRNA TP73-AS1 and BDH2 levels are generally upregulated in esophageal cancer tissues and are strongly correlated with tumor location or TNM stage in clinical samples. LncRNA TP73-AS1 knockdown inhibited BDH2 expression in EC9706 and KYSE30 cells, whereas BDH2 knockdown repressed esophageal cancer cell proliferation and induced apoptosis via the caspase-3 dependent apoptotic pathway. Overexpression of BDH2 in lncRNA TP73-AS1 knockdown cells partially rescued cell proliferation rates and suppressed apoptosis. In mouse xenografts, tumor size was reduced in lncRNA TP73-ASI siRNA-transfected tumors, suggesting that downregulation of lncRNA TP73-AS1 attenuated EC proliferation in vitro and in vivo. In addition, BDH2 or lncRNA TP73-AS1 knockdown enhanced the chemosensitivity of esophageal cancer cells to 5-FU and cisplatin. Our results suggest that lncRNA TP73-AS1 may be a novel prognostic biomarker that could serve as a potential therapeutic target for the treatment of esophageal cancer.

microRNA-186 inhibits cell proliferation and induces apoptosis in human esophageal squamous cell carcinoma by targeting SKP2.

miR-186 has been demonstrated to have a significant role as a tumor suppressor in many types of cancers. Nevertheless, its biological function in esophageal squamous cell carcinoma (ESCC) remains unknown. In the present study, we found that the expression level of miR-186 was downregulated in ESCC in comparison with the adjacent normal tissues and was significantly associated with differentiation level, TNM stage, and lymph node metastasis of ESCC. Functional experiments revealed that enforced overexpression of miR-186 in ESCC cells suppressed the proliferation, invasion, and induced the apoptosis of cells. Luciferase reporter assay and western blotting analysis were performed to verify the target gene regulated by miR-186, SKP2. Our findings established that the miR-186 has a suppressive role in ESCC progression via SKP2-mediated pathway, and this implies that miR-186 could be a potential therapeutic target for ESCC.