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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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      Tumor suppressive functions of LZTFL1 in hepatocellular carcinoma

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          Abstract

          Background: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related mortality worldwide. The poor survival may be due to tumor recurrence and metastasis. Growing evidence indicates that Leucine Zipper Transcription Factor-like 1 ( LZTFL1) plays an important role in tumor progression of several cancers such as lung cancer and gastric cancer.

          Methods: Real-time PCR was performed to evaluate LZTFL1 expression level in HCC cell lines and patient specimens. The relationship between LZTFL1 expression and the clinicopathological data of the patients was analyzed. Stable cell lines with overexpressing LZTFL1 were set-up, and the cell proliferation, migration, and invasion abilities were analyzed. The protein expression was measured by Western blotting.

          Results: Here, we found LZTFL1 expression was decreased in human HCC specimens and HCC cell lines. Downregulation of LZTFL1 expression was correlated with tumor stage and metastasis. The ectopic overexpression of LZTFL1 inhibited cell proliferation, migration, invasion, and the expression of MMP9. In addition, LZTFL1 suppressed epithelial mesenchymal transition (EMT).

          Conclusion: Taken together, our results highlight the tumor suppressive role of LZTFL1 in HCC, suggesting that LZTFL1 may represent a potential therapeutic strategy for treating patients with HCC.

          Most cited references16

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          New insights into the mechanisms of epithelial–mesenchymal transition and implications for cancer

          Epithelial-mesenchymal transition (EMT) is a cellular programme that is known to be crucial for embryogenesis, wound healing and malignant progression. During EMT, cell-cell and cell-extracellular matrix interactions are remodelled, which leads to the detachment of epithelial cells from each other and the underlying basement membrane, and a new transcriptional programme is activated to promote the mesenchymal fate. In the context of neoplasias, EMT confers on cancer cells increased tumour-initiating and metastatic potential and a greater resistance to elimination by several therapeutic regimens. In this Review, we discuss recent findings on the mechanisms and roles of EMT in normal and neoplastic tissues, and the cell-intrinsic signals that sustain expression of this programme. We also highlight how EMT gives rise to a variety of intermediate cell states between the epithelial and the mesenchymal state, which could function as cancer stem cells. In addition, we describe the contributions of the tumour microenvironment in inducing EMT and the effects of EMT on the immunobiology of carcinomas.
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            Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma

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              Tumor mutational burden is a determinant of immune-mediated survival in breast cancer

              ABSTRACT Mounting evidence supports a role for the immune system in breast cancer outcomes. The ability to distinguish highly immunogenic tumors susceptible to anti-tumor immunity from weakly immunogenic or inherently immune-resistant tumors would guide development of therapeutic strategies in breast cancer. Genomic, transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) breast cancer cohorts were used to examine statistical associations between tumor mutational burden (TMB) and the survival of patients whose tumors were assigned to previously-described prognostic immune subclasses reflecting favorable, weak or poor immune-infiltrate dispositions (FID, WID or PID, respectively). Tumor immune subclasses were associated with survival in patients with high TMB (TMB-Hi, P < 0.001) but not in those with low TMB (TMB-Lo, P = 0.44). This statistical relationship was confirmed in the METABRIC cohort (TMB-Hi, P = 0.047; TMB-Lo, P = 0.39), and also found to hold true in the more-indolent Luminal A tumor subtype (TMB-Hi, P = 0.011; TMB-Lo, P = 0.91). In TMB-Hi tumors, the FID subclass was associated with prolonged survival independent of tumor stage, molecular subtype, age and treatment. Copy number analysis revealed the reproducible, preferential amplification of chromosome 1q immune-regulatory genes in the PID immune subclass. These findings demonstrate a previously unappreciated role for TMB as a determinant of immune-mediated survival of breast cancer patients and identify candidate immune-regulatory mechanisms associated with immunologically cold tumors. Immune subtyping of breast cancers may offer opportunities for therapeutic stratification.
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                Author and article information

                Journal
                Onco Targets Ther
                Onco Targets Ther
                OTT
                ott
                OncoTargets and therapy
                Dove
                1178-6930
                10 July 2019
                2019
                : 12
                : 5537-5544
                Affiliations
                [1 ]Department of Infectious Disease, The First Affiliated Hospital of Zhengzhou University , Zhengzhou 450052, Henan, People’s Republic of China
                Author notes
                Correspondence: Zujiang YuDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University , 1st Jianshe Road, Zhengzhou450052, Henan, People’s Republic of ChinaEmail johnyuem@ 123456zzu.edu.cn
                [*]

                These authors contributed equally to this work

                Article
                196925
                10.2147/OTT.S196925
                6628092
                53631f7b-2f79-49e3-b598-da84811de36b
                © 2019 Li et al.

                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
                : 04 December 2018
                : 04 March 2019
                Page count
                Figures: 5, Tables: 1, References: 23, Pages: 8
                Categories
                Original Research

                Oncology & Radiotherapy
                hepatocellular carcinoma, hcc,lztfl1,migration and invasion,epithelial mesenchymal transition, emt

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