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      Potential Role of DEC1 in Cervical Cancer Cells Involving Overexpression and Apoptosis

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          Abstract

          Basic helix-loop-helix (BHLH) transcription factors differentiated embryonic chondrocyte gene 1 (DEC1) and gene 2 (DEC2) regulate circadian rhythms, apoptosis, epithelial mesenchymal transition (EMT), invasions and metastases in various kinds of cancer. The stem cell markers SOX2 and c-MYC are involved in the regulation of apoptosis and poor prognosis. In cervical cancer, however, their roles are not well elucidated yet. To determine the function of these genes in human cervical cancer, we examined the expression of DEC1, DEC2, SOX2 and c-MYC in human cervical cancer tissues. In immunohistochemistry, they were strongly expressed in cancer cells compared with in non-cancerous cells. Notably, the strong rate of DEC1 and SOX2 expressions were over 80% among 20 cases. We further examined the roles of DEC1 and DEC2 in apoptosis. Human cervical cancer HeLa and SiHa cells were treated with cisplatin—HeLa cells were sensitive to apoptosis, but SiHa cells were resistant. DEC1 expression decreased in the cisplatin-treated HeLa cells, but had little effect on SiHa cells. Combination treatment of DEC1 overexpression and cisplatin inhibited apoptosis and affected SOX2 and c-MYC expressions in HeLa cells. Meanwhile, DEC2 overexpression had little effect on apoptosis and on SOX2 and c-MYC expressions. We conclude that DEC1 has anti-apoptotic effects and regulates SOX2 and c-MYC expressions on apoptosis.

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          Most cited references 40

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          Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method.

          The two most commonly used methods to analyze data from real-time, quantitative PCR experiments are absolute quantification and relative quantification. Absolute quantification determines the input copy number, usually by relating the PCR signal to a standard curve. Relative quantification relates the PCR signal of the target transcript in a treatment group to that of another sample such as an untreated control. The 2(-Delta Delta C(T)) method is a convenient way to analyze the relative changes in gene expression from real-time quantitative PCR experiments. The purpose of this report is to present the derivation, assumptions, and applications of the 2(-Delta Delta C(T)) method. In addition, we present the derivation and applications of two variations of the 2(-Delta Delta C(T)) method that may be useful in the analysis of real-time, quantitative PCR data. Copyright 2001 Elsevier Science (USA).
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            SOX2 Gene Regulates the Transcriptional Network of Oncogenes and Affects Tumorigenesis of Human Lung Cancer Cells

            Recent studies demonstrated that cancer stem cells (CSCs) have higher tumorigenesis properties than those of differentiated cancer cells and that transcriptional factor-SOX2 plays a vital role in maintaining the unique properties of CSCs; however, the function and underlying mechanism of SOX2 in carcinogenesis of lung cancer are still elusive. This study applied immunohistochemistry to analyze the expression of SOX2 in human lung tissues of normal individuals as well as patients with adenocarcinoma, squamous cell carcinoma, and large cell and small cell carcinoma and demonstrated specific overexpression of SOX2 in all types of lung cancer tissues. This finding supports the notion that SOX2 contributes to the tumorigenesis of lung cancer cells and can be used as a diagnostic probe. In addition, obviously higher expression of oncogenes c-MYC, WNT1, WNT2, and NOTCH1 was detected in side population (SP) cells than in non-side population (NSP) cells of human lung adenocarcinoma cell line-A549, revealing a possible mechanism for the tenacious tumorigenic potential of CSCs. To further elucidate the function of SOX2 in tumorigenesis of cancer cells, A549 cells were established with expression of luciferase and doxycycline-inducible shRNA targeting SOX2. We found silencing of SOX2 gene reduces the tumorigenic property of A549 cells with attenuated expression of c-MYC, WNT1, WNT2, and NOTCH1 in xenografted NOD/SCID mice. By using the RNA-Seq method, an additional 246 target cancer genes of SOX2 were revealed. These results present evidence that SOX2 may regulate the expression of oncogenes in CSCs to promote the development of human lung cancer.
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              Chemotherapy for recurrent cervical cancer.

              Cervical cancer is the second most common cancer of women worldwide and one of the leading cause of death in relative young women. This review gives an outline of chemotherapy of advanced, persistent or recurrent cervical cancer. We performed a literature search in the PubMed of almost all relevant articles concerning chemotherapy of advanced, persistent or recurrent cervical cancer. The available data from the literature is mainly composed of most recent reviews, phase II and randomized phase III clinical trials. Single-agent cisplatin remains the current standard therapy for advanced, persistent or recurrent cervical cancer. Several single-agents have been tested, but none has been found to be superior compared to cisplatin. Both topotecan and paclitaxel in combination with cisplatin, have yielded superior response rates and progression-free survival without diminishing patient quality of life. However, only the combination of cisplatin and topotecan has improved overall survival. It is important to identify clinical and tumor-related factors predictive of response to cisplatin-based chemotherapy. Future trials are necessary, not only to compare combinations of existing agents, but to incorporate biological agents (monoclonal antibodies or small molecules) to chemotherapy in order to improve the treatment results of advanced, persistent or recurrent cervix cancer.
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                Author and article information

                Journal
                Clocks Sleep
                Clocks Sleep
                clockssleep
                Clocks & Sleep
                MDPI
                2624-5175
                26 January 2020
                March 2020
                : 2
                : 1
                : 26-38
                Affiliations
                [1 ]Department of Pathology, Wakayama Medical University School of Medicine, Wakayama 641-8509, Japan; d1666040@ 123456wakayama-med.ac.jp (N.S.); osakipon@ 123456gmail.com (S.O.); k-oikawa@ 123456wakayama-med.ac.jp (K.O.); ymuragak@ 123456wakayama-med.ac.jp (Y.M.)
                [2 ]Department of Diagnostic Pathology, Shizuoka Cancer Center, Sunto-gun 411-8777, Japan
                [3 ]Department of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo, Chiba 271-8587, Japan; bhawal.ujjal.kumar@ 123456nihon-u.ac.jp
                Author notes
                [* ]Correspondence: fsatoDEC1DEC2@ 123456yahoo.co.jp ; Tel.: +81-73-441-0634; Fax: +81-73-446-3781
                [†]

                These authors contributed equally to this work.

                Article
                clockssleep-02-00004
                10.3390/clockssleep2010004
                7445836
                33089188
                © 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/).

                Categories
                Article

                dec1, sox2, c-myc, immunohistochemistry, cervical cancer

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