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Lloyd Tanner posted an update 6 months ago
In addition, CSC‑like properties, including the expression of CD133, CD44, sex determining region Y‑box 2, Nanog and octamer‑binding transcription factor 4, were markedly decreased in the A549 and H1299 sphere cells following knockdown of CLOCK. Epigallocatechin‑3‑gallate (EGCG), a green tea polyphenol, has been reported to be a potential anticancer phytochemical. EGCG was found to repress CLOCK expression in A549 and H1299 sphere cells. In addition, EGCG also decreased the ratio of CD133+ cells. The Wnt/β‑catenin pathway was notably inactivated by the knockdown of CLOCK in A549 and H1299 sphere cells. Subsequently, using a xenograft model, it was demonstrated that EGCG suppressed the CSC‑like characteristics of lung cancer cells by targeting CLOCK. In conclusion, the present study demonstrated that EGCG inhibited the self‑renewal ability of lung cancer stem‑like cells by targeting CLOCK.After the publication of the above article, the authors have realized that Figs. 2 and 4 in their paper were published with incorrect images; regarding Fig. 2, the data featured in Fig. 2A (for the H/SD + Nico 1000 µM panel) were repeated with those featured in Fig. 1C (the 6 h H/SD panel), and the data shown for Bcl-2 in Fig. 4C were selected incorrectly. These errors arose inadvertently as a consequence of misassembling the figures. The revised versions of Figs. 2 and 4, featuring the corrected data panels for the above‑mentioned experiments, are shown on the next page. Note that the revised data shown for these Figures do not affect the overall conclusions reported in the paper. The authors express their gratitude to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. .Annexin IV (ANXA4) is highly expressed in ovarian clear cell carcinoma (OCCC); however, its underlying molecular mechanism in OCCC remains unknown. The present study aimed to identify the molecule that ANXA4 may act on and to determine its underlying molecular mechanism. Immunohistochemistry, co‑immunoprecipitation and western blotting were performed to detect the expression and interaction of ANXA4, and its associated proteins. Furthermore, MTT assay, flow cytometry, western blotting and gene expression profile enrichment analysis were performed to identify the potential role and molecular mechanism of ANXA4 in OCCC. The results demonstrated that ANXA4 and nuclear factor‑κ‑light‑chain‑enhancer of activated B cells (NF‑κB) p50 nuclear expression levels were significantly higher in OCCC tissues compared with other subtypes of ovarian cancer, such as serous and mucinous. In addition, a significantly positive correlation was observed between ANXA4 and NF‑κB p50 expression in OCCC; however, the expression levels raction. This in turn activates the NF‑κB signaling pathway, promotes cell cycle progression and inhibits apoptosis, thus contributing to the malignant progression of OCCC. Thus, ANXA4 and NF‑κB p50 may be used as prognostic biomarkers, and may be molecular therapeutic targets in OCCC.The authors of the above article drew to our attention that, in the above paper, they had identified three instances of data overlapping between data panels, suggesting that data purportedly showing results obtained under different experimental conditions had been derived from the same original source. Comparing among the data panels, two pairs of panels in Fig. 4B were shown to be overlapping, and a further pair of panels showed overlapping data in Fig. 6B. The authors were presented with an opportunity to correct their figures in a Corrigendum, although it has subsequently come to light that the replacement figures themselves featured problems with overlapping data. Given the errors that have been identified in the compilation of the figures in this article, the Editor of Oncology Reports has decided that this article should be retracted from the publication owing to a lack of overall confidence in the presented data. The authors all agree to the retraction of this article, and the Editor and the authors apologize for any inconvenience that might result from this retraction. .During the preparation of the figures in the above article, the authors regret that errors occurred during the assembly of Figs. 3, 5 and 6. An incorrect image for the calcein‑AM/PI staining data panel for nHC and transforming growth factor‑β (TGF‑β) group at 6 days was shown in Fig. 3A; similarly, in both Figs. 5A and 6, images were selected incorrectly for safranin O and collagen type Ⅱ (COL II) staining for the hydroxyapatite/collagen (HC) group at 4 and 6 days, and also COL Ⅱ staining for the TGF‑β group at 4 days in Fig. 6. Each of these errors were attributed to an accidental mix‑up of the data during the image compilation process. Corrected versions of Figs. 3, 5 and 6 are shown on the next two pages. These errors did not affect the major conclusions reported in the paper. this website All the authors have agreed to this Corrigendum, and thank the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this. The authors regret these errors went unnoticed during the compilation of the three figures in question, and apologize to the readership for any confusion that it may have caused. .As a novel halogenated hydroxyl ether‑inhaled general anesthetic, sevoflurane has been reported to affect the progression of diverse human cancers. In the present study, we aimed to explore the functions and underlying mechanisms of sevoflurane in colon cancer. MTT assay, flow cytometric analysis and Transwell assay were conducted to evaluate cell viability, apoptosis and invasion, respectively. Western blot analysis was performed to determine the protein level of sphingosine‑1‑phosphate phosphatase 1 (SGPP1). The morphology and size of exosomes were analyzed by TEM and NTA. The levels of circular RNA 3‑hydroxy‑3‑methylglutaryl‑CoA synthase 1 (circ‑HMGCS1), microRNA (miR)‑34a‑5p and SGPP1 mRNA were examined by RT‑qPCR. Dual‑luciferase reporter and RNA RIP assays were utilized to explore the interaction between miR‑34a‑5p and circ‑HMGCS1 or SGPP1. A murine xenograft model was established to investigate the effect of circ‑HMGCS1 in vivo. As a result, it was determined that sevoflurane suppressed cell viability and invasion and induced apoptosis in colon cancer in a dose‑dependent way.
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