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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      Curcumin reverses oxaliplatin resistance in human colorectal cancer via regulation of TGF-β/Smad2/3 signaling pathway

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background: Oxaliplatin (OXA) resistance is a main obstacle to the chemotherapy of colorectal cancer (CRC). Epithelial-mesenchymal transition (EMT), which is mainly regulated by TGF-β/Smad signaling pathway, has gradually been recognized as an important mechanism for tumor chemoresistance. Studies have shown that curcumin regulated EMT processes in many human cancers. However, whether curcumin could regulate OXA resistance in CRC through modulating TGF-β/Smad signaling-mediated EMT remains unclear.

          Methods: In an attempt to investigate the effect of curcumin on OXA resistance in CRC, OXA-resistant cell line HCT116/OXA was established firstly. The effect of curcumin on cell proliferation was evaluated by MTT assay and Ki67 immunofluorescence staining, respectively. Cell apoptosis was evaluated by flow cytometry. In addition, transwell assay was used to detect the effect of curcumin on cell invasion and the activation of TGF-β/Smad signaling was examined by immunofluorescence and Western blot. Moreover, the therapeutic potential of curcumin was further examined in vivo using a CRC animal model.

          Results: The OXA-resistant cell line HCT116/OXA was successfully established, and combination of OXA with curcumin reduced OXA resistance in vitro. Besides, the combination treatment inhibited the expressions of p-p65 and Bcl-2, but increased the level of active-caspase3. In addition, curcumin inhibited EMT via regulation of TGF-β/Smad2/3 signaling pathway. Moreover, in vivo study confirmed curcumin could reverse OXA resistance in CRC.

          Conclusion: Our study indicated that curcumin could reserve OXA resistance in CRC through dampening TGF-β/Smads signaling in vitro and in vivo.

          Most cited references29

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          The Essential Medicinal Chemistry of Curcumin

          Kathryn Nelson, Jayme L Dahlin, Jonathan Bisson … (2017)
          Curcumin is a constituent (up to ∼5%) of the traditional medicine known as turmeric. Interest in the therapeutic use of turmeric and the relative ease of isolation of curcuminoids has led to their extensive investigation. Curcumin has recently been classified as both a PAINS (pan-assay interference compounds) and an IMPS (invalid metabolic panaceas) candidate. The likely false activity of curcumin in vitro and in vivo has resulted in >120 clinical trials of curcuminoids against several diseases. No double-blinded, placebo controlled clinical trial of curcumin has been successful. This manuscript reviews the essential medicinal chemistry of curcumin and provides evidence that curcumin is an unstable, reactive, nonbioavailable compound and, therefore, a highly improbable lead. On the basis of this in-depth evaluation, potential new directions for research on curcuminoids are discussed.
          Article 0 comments Cited 334 times – based on 0 reviews     Review now
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            Multi-drug resistance in cancer chemotherapeutics: mechanisms and lab approaches.

            Qiong Wu, Zhiping Yang, Yongzhan Nie … (2014)
            Multi-drug resistance (MDR) has become the largest obstacle to the success of cancer chemotherapies. The mechanisms of MDR and the approaches to test MDR have been discovered, yet not fully understood. This review covers the in vivo and in vitro approaches for the detection of MDR in the laboratory and the mechanisms of MDR in cancers. This study also envisages the future developments toward the clinical and therapeutic applications of MDR in cancer treatment. Future therapeutics for cancer treatment will likely combine the existing therapies with drugs originated from MDR mechanisms such as anti-cancer stem cell drugs, anti-miRNA drugs or anti-epigenetic drugs. The challenges for the clinical detection of MDR will be to find new biomarkers and to determine new evaluation systems before the drug resistance emerges. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
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              Twist transcriptionally up-regulates AKT2 in breast cancer cells leading to increased migration, invasion, and resistance to paclitaxel.

              George Z Cheng, Joseph Chan, Qi Wang … (2007)
              Metastasis, the cardinal feature of malignant tumors, is an important clinical variable in patient prognosis. To understand the basis for metastasis, we systematically selected for highly invasive cells from breast cancer cell lines, MCF7 and MDA-MB-453, with moderate to low invasive ability using Boyden chamber invasion assay. The four-cycle selected invasive lines, named MCF7-I4 and MDA-MB-453-I4, respectively, displayed epithelial-mesenchymal transition (EMT) and dramatically enhanced invasive ability. EMT changes were corroborated with decreased level of E-cadherin and increased vimentin, fibronectin, and beta(1) integrin. Twist, a basic helix-loop-helix transcription factor, and AKT2, a known proto-oncogene, were found to be elevated in the invasive cells compared with the parental. Ectopic expression and knockdown of Twist by short interference RNA resulted in significant increase and reduction, respectively, of AKT2 protein and mRNA expression. Twist bound to E-box elements on AKT2 promoter and enhanced its transcriptional activity. Moreover, silencing AKT2 decreased Twist-promoted migration, invasion, and paclitaxel resistance. Reintroducing AKT2 largely rescued the phenotype resulted from knockdown of Twist in I4 cells, suggesting that AKT2 is a downstream target and functional mediator of Twist. Finally, we observed a 68.8% correlation of elevated Twist and AKT2 expression in late-stage breast cancers as oppose to 13% in early-stage breast cancers. Our study identifies Twist as a positive transcriptional regulator of AKT2 expression, and Twist-AKT2 signaling is involved in promoting invasive ability and survival of breast cancer cells.
              Article 0 comments Cited 185 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): OTT
                Journal ID (pmc): ott
                Title: OncoTargets and therapy
                Publisher: Dove
                ISSN (Electronic): 1178-6930
                Publication date (Electronic): 17 May 2019
                Publication date Collection: 2019
                Volume: 12
                Pages: 3893-3903
                Affiliations
                [1 ]Department of General Surgery, Shanghai Luodian Hospital , Shanghai 201908, People’s Republic of China
                [2 ]Department of Gynaecology and Obstetrics, Shanghai Luodian Hospital , Shanghai 201908, People’s Republic of China
                Author notes
                Correspondence: Lei WuDepartment of General Surgery, Shanghai Luodian Hospital , No.121 Luoxi Road, Luodian Town, Baoshan District, Shanghai201908, People’s Republic of ChinaEmail lei_wu212@ 123456126.com
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 199601
                DOI: 10.2147/OTT.S199601
                PMC ID: 6529728
                PubMed ID: 31190888
                SO-VID: 4baee1d3-9866-445a-8f9c-65a96165bf3e
                Copyright © © 2019 Yin et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 26 December 2018
                Date accepted : 11 April 2019
                Page count
                Figures: 6, Tables: 1, References: 39, Pages: 11
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: colorectal cancer,oxaliplatin resistance,curcumin,epithelial-mesenchymal transition,tgf-β/smad signaling pathway
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: colorectal cancer, oxaliplatin resistance, curcumin, epithelial-mesenchymal transition, tgf-β/smad signaling pathway

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