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      Author Correction: Novel Indole-fused benzo-oxazepines (IFBOs) inhibit invasion of hepatocellular carcinoma by targeting IL-6 mediated JAK2/STAT3 oncogenic signals

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          Abstract

          Correction to: Scientific Reports 10.1038/s41598-018-24288-0, published online 12 April 2018 This Article contains errors. The Legend for Figure 6 is incomplete, as it does not specify that the control data has been published in Figure 6 of a previous study 1 ; these two studies were performed simultaneously, with the same normal control, positive control, and negative control groups. The Supplementary Information did not include full-length gel images. Uncropped images for Figure 4B are provided below as Figure 1. Figure 1 .

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          5H-benzo[h]thiazolo[2,3-b]quinazolines ameliorate NDEA-induced hepatocellular carcinogenesis in rats through IL-6 downregulation along with oxidative and metabolic stress reduction

          5H-benzo[h]thiazolo[2,3-b]quinazoline scaffold is known to have an antitumor effect on certain types of malignancies; however, its effect on hepatocellular carcinoma (HCC) remains unclear. Previously, we reported p-toluenesulfonic acid-promoted syntheses, molecular modeling and in vitro antitumor activity of 5H-benzo[h]thiazolo[2,3-b]quinazoline against human hepatoma (Hep-G2) cells where compounds 4A and 6A were found to be potent inhibitors among the series. In continuation to our previous effort to develop novel therapeutic strategies for HCC treatment, here we investigated the in vivo antitumor activity and the mechanism underlying the effects of 4A and 6A in N-nitrosodiethylamine (NDEA)-induced HCC using male Wistar rats. NDEA was administered weekly intraperitoneally at a dose of 100 mg/kg for 6 weeks. Various physiological and morphological changes, oxidative parameters, liver marker enzymes and cytokines were assessed to evaluate the antitumor effect of 4A and 6A. In addition, proton nuclear magnetic resonance-based serum metabolomics were performed to analyze the effects of 4A and 6A against HCC-induced metabolic alterations. Significant tumor incidences with an imbalance in carcinogen metabolizing enzymes and cellular redox status were observed in carcinogenic rats. Tumor inhibitory effects of 4A and 6A were noted by histopathology and biochemical profiles in NDEA-induced hepatic cancer. Compounds 4A and 6A had a potential role in normalizing the elevated levels of inflammatory mediators such as interleukin-1β (IL-1β), IL-2, IL-6 and IL-10. At molecular level, the real-time quantitative reverse-transcribed polymerase chain reaction analysis revealed that 4A and 6A attenuated the IL-6 gene overexpression in hepatic cancer. Further, orthogonal partial least squares discriminant analysis scores plot demonstrated a significant separation of 4A and 6A-treated groups from carcinogen control group. Both the compounds have potential to restore the imbalanced metabolites due to HCC, signifying promising hepatoprotective activities. All these findings suggested that 4A and 6A could be potential drug candidates to treat HCC.
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            Author and article information

            Contributors
            sudiptapharm@gmail.com
            Journal
            Sci Rep
            Sci Rep
            Scientific Reports
            Nature Publishing Group UK (London )
            2045-2322
            6 February 2020
            6 February 2020
            2020
            : 10
            : 2391
            Affiliations
            [1 ]GRID grid.440550.0, Department of Pharmaceutical Sciences, , Babasaheb Bhimrao Ambedkar University, ; Vidya Vihar, Raibareli Road, Lucknow, 226025 India
            [2 ]ISNI 0000 0004 1781 2531, GRID grid.459970.6, Faculty of Mathematical and Statistical Sciences, , Shri Ramswaroop Memorial University, ; Deva Road, Lucknow, 225003 India
            [3 ]ISNI 0000 0000 9346 7267, GRID grid.263138.d, Centre of Biomedical Research, SGPGIMS Campus, ; Raebareli Road, Lucknow, 226014 Uttar Pradesh India
            [4 ]GRID grid.440550.0, Department of Biotechnology, , Babasaheb Bhimrao Ambedkar University, ; Vidya Vihar, Raibareli Road, Lucknow, 226025 India
            Article
            59134
            10.1038/s41598-020-59134-9
            7002741
            32024920
            9967203d-25e5-4668-b8b2-bdf0e47da4b7
            © The Author(s) 2020

            Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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