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      Role of SOX Protein Groups F and H in Lung Cancer Progression

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          Abstract

          Simple Summary

          The expression of SOX proteins has been demonstrated in many tissues at various stages of embryogenesis, where they play the role of transcription factors. The SOX18 protein (along with SOX7 and SOX17) belongs to the SOXF group and is mainly involved in the development of the cardiovascular system, where its expression was found in the endothelium. SOX18 expression was also demonstrated in neoplastic lines of gastric, pancreatic and colon adenocarcinomas. The prognostic role of SOX30 expression has only been studied in lung adenocarcinomas, where a low expression of this factor in the stromal tumor was associated with a worse prognosis for patients. Because of the complexity of non-small-cell lung cancer (NSCLC) development, the role of the SOX proteins in this malignancy is still not fully understood. Many recently published papers show that SOX family protein members play a crucial role in the progression of NSCLC.

          Abstract

          The SOX family proteins are proved to play a crucial role in the development of the lymphatic ducts and the cardiovascular system. Moreover, an increased expression level of the SOX18 protein has been found in many malignances, such as melanoma, stomach, pancreatic breast and lung cancers. Another SOX family protein, the SOX30 transcription factor, is responsible for the development of male germ cells. Additionally, recent studies have shown its proapoptotic character in non-small cell lung cancer cells. Our preliminary studies showed a disparity in the amount of mRNA of the SOX18 gene relative to the amount of protein. This is why our attention has been focused on microRNA (miRNA) molecules, which could regulate the SOX18 gene transcript level. Recent data point to the fact that, in practically all types of cancer, hundreds of genes exhibit an abnormal methylation, covering around 5–10% of the thousands of CpG islands present in the promoter sequences, which in normal cells should not be methylated from the moment the embryo finishes its development. It has been demonstrated that in non-small-cell lung cancer (NSCLC) cases there is a large heterogeneity of the methylation process. The role of the SOX18 and SOX30 expression in non-small-cell lung cancers (NSCLCs) is not yet fully understood. However, if we take into account previous reports, these proteins may be important factors in the development and progression of these malignancies.

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          Hallmarks of Cancer: The Next Generation

          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Wnt/beta-catenin signaling: components, mechanisms, and diseases.

            Signaling by the Wnt family of secreted glycolipoproteins via the transcriptional coactivator beta-catenin controls embryonic development and adult homeostasis. Here we review recent progress in this so-called canonical Wnt signaling pathway. We discuss Wnt ligands, agonists, and antagonists, and their interactions with Wnt receptors. We also dissect critical events that regulate beta-catenin stability, from Wnt receptors to the cytoplasmic beta-catenin destruction complex, and nuclear machinery that mediates beta-catenin-dependent transcription. Finally, we highlight some key aspects of Wnt/beta-catenin signaling in human diseases including congenital malformations, cancer, and osteoporosis, and discuss potential therapeutic implications.
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              • Record: found
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              Lung Cancer 2020

              Despite advances in our understanding of risk, development, immunologic control, and treatment options for lung cancer, it remains the leading cause of cancer death. Tobacco smoking remains the predominant risk factor for lung cancer development. Nontobacco risk factors include environmental and occupational exposures, chronic lung disease, lung infections, and lifestyle factors. Because tobacco remains the leading risk factor for lung cancer, disease prevention is focused on smoking avoidance and cessation. Other prevention measures include healthy diet choices and maintaining a physically active lifestyle. Future work should focus on smoking cessation campaigns and better understanding disease development and treatment strategies in nonsmokers.
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                Author and article information

                Journal
                Cancers (Basel)
                Cancers (Basel)
                cancers
                Cancers
                MDPI
                2072-6694
                03 November 2020
                November 2020
                : 12
                : 11
                : 3235
                Affiliations
                [1 ]Department of Histology and Embryology, Department of Human Morphology and Embryology, Medical University, 50-368 Wroclaw, Poland; piotr.dziegiel@ 123456umed.wroc.pl
                [2 ]Department of Ultrastructural Research, Department of Human Morphology and Embryology, Medical University, 50-368 Wroclaw, Poland; marzenna.podhorska-okolow@ 123456umed.wroc.pl
                [3 ]Department of Physiotherapy, University School of Physical Education, 51-612 Wroclaw, Poland
                Author notes
                [* ]Correspondence: mateusz.olbromski@ 123456umed.wroc.pl ; Tel.: +48-717-841-354; Fax: +48-717-840-082
                Author information
                https://orcid.org/0000-0002-8292-1385
                Article
                cancers-12-03235
                10.3390/cancers12113235
                7692225
                33152990
                feaa9076-d2f0-47c1-9725-35902aac7966
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 09 October 2020
                : 27 October 2020
                Categories
                Review

                non-small cell lung carcinoma,lung squamous-cell carcinoma,lung adenocarcinoma,sox protein family,sox7,sox17,sox18,sox30,mirna,cpg

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