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Cancers
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The Role of SOX Transcription Factors in Cancer
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The Role of SOX Transcription Factors in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 9553

Special Issue Editors

Dr. Philippe Blache

E-Mail Website
Guest Editor
Institut de Recherche en Cancérologie de Montpellier (IRCM), University of Montpellier, ICM, INSERM U1194, Montpellier, France
Interests: SOX9 transcription factor; colorectal cancer; oncogene; tumor suppressor; wnt/beta-catenin signaling pathway; circulating nucleic acid
Dr. Corinne Prévostel

E-Mail Website
Guest Editor
Institut de Recherche en Cancérologie de Montpellier (IRCM), University of Montpellier, ICM, INSERM U1194, Montpellier, France
Interests: protein kinase Cα; tumor suppressor; nanovector; SOX9 transcription factor; colorectal cancer; wnt/beta-catenin signaling; therapeutic peptides
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

SOX transcription factors contain a high mobility group (HMG) domain, a conserved amino acid sequence that was originally identified in Sry, a transcription factor that is essential for male sex determination. The SOX family comprises more than 20 members and is recognized as a key element in the development of many organs. It is now clear that SOX proteins also play important roles in the development of many human cancers. Some SOX are oncogenes, others are tumor suppressors, and others can be either oncogenes or tumor suppressors depending on the context. In this Special Issue of Cancers, we intend to highlight the complex, paradoxical, and fascinating roles of SOX in several types of cancer. We aim to cover both fundamental and clinical aspects of this field in order to provide an overview of the mechanisms of action of SOX transcription factors and their clinical potential in the management of human cancers.

Dr. Philippe Blache
Dr. Corinne Prévostel
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • SOX transcription factors
  • cancer
  • signaling pathway
  • oncogene
  • tumor suppressor
  • biomarker

Published Papers (3 papers)

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Research

16 pages, 3891 KiB  
Article
RIP140 Represses Intestinal Paneth Cell Differentiation and Interplays with SOX9 Signaling in Colorectal Cancer
by Antoine Gleizes, Mouna Triki, Sandrine Bonnet, Naomi Baccari, Gabriel Jimenez-Dominguez, Aurélie Covinhes, Nelly Pirot, Philippe Blache, Rong Yuan, Balázs Győrffy, Vincent Cavaillès and Marion Lapierre
Cancers 2021, 13(13), 3192; https://doi.org/10.3390/cancers13133192 - 26 Jun 2021
Cited by 3 | Viewed by 3140
Abstract
RIP140 is a major transcriptional coregulator of gut homeostasis and tumorigenesis through the regulation of Wnt/APC signaling. Here, we investigated the effect of RIP140 on Paneth cell differentiation and its interplay with the transcription factor SOX9. Using loss of function mouse models, human [...] Read more.
RIP140 is a major transcriptional coregulator of gut homeostasis and tumorigenesis through the regulation of Wnt/APC signaling. Here, we investigated the effect of RIP140 on Paneth cell differentiation and its interplay with the transcription factor SOX9. Using loss of function mouse models, human colon cancer cells, and tumor microarray data sets we evaluated the role of RIP140 in SOX9 expression and activity using RT-qPCR, immunohistochemistry, luciferase reporter assays, and GST-pull down. We first evidence that RIP140 strongly represses the Paneth cell lineage in the intestinal epithelium cells by inhibiting Sox9 expression. We then demonstrate that RIP140 interacts with SOX9 and inhibits its transcriptional activity. Our results reveal that the Wnt signaling pathway exerts an opposite regulation on SOX9 and RIP140. Finally, the levels of expression of RIP140 and SOX9 exhibit a reverse response and prognosis value in human colorectal cancer biopsies. This work highlights an intimate transcriptional cross-talk between RIP140 and SOX9 in intestinal physiopathology. Full article
(This article belongs to the Special Issue The Role of SOX Transcription Factors in Cancer)
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16 pages, 5953 KiB  
Article
CRISPR/Cas9 Deletion of SOX2 Regulatory Region 2 (SRR2) Decreases SOX2 Malignant Activity in Glioblastoma
by Ander Saenz-Antoñanzas, Veronica Moncho-Amor, Jaione Auzmendi-Iriarte, Alejandro Elua-Pinin, Karine Rizzoti, Robin Lovell-Badge and Ander Matheu
Cancers 2021, 13(7), 1574; https://doi.org/10.3390/cancers13071574 - 29 Mar 2021
Cited by 8 | Viewed by 2710
Abstract
SOX2 is a transcription factor associated with stem cell activity in several tissues. In cancer, SOX2 expression is increased in samples from several malignancies, including glioblastoma, and high SOX2 levels are associated with the population of tumor-initiating cells and with poor patient outcome. [...] Read more.
SOX2 is a transcription factor associated with stem cell activity in several tissues. In cancer, SOX2 expression is increased in samples from several malignancies, including glioblastoma, and high SOX2 levels are associated with the population of tumor-initiating cells and with poor patient outcome. Therefore, understanding how SOX2 is regulated in cancer cells is relevant to tackle tumorigenesis. The SOX2 regulatory region 2(SRR2) is located downstream of the SOX2 coding region and mediates SOX2 expression in embryonic and adult stem cells. In this study, we deleted SRR2 using CRISPR/Cas9 in glioblastoma cells. Importantly, SRR2-deleted glioblastoma cells presented reduced SOX2 expression and decreased proliferative activity and self-renewal capacity in vitro. In line with these results, SRR2-deleted glioblastoma cells displayed decreased tumor initiation and growth in vivo. These effects correlated with an elevation of p21CIP1 cell cycle and p27KIP1 quiescence regulators. In conclusion, our data reveal that SRR2 deletion halts malignant activity of SOX2 and confirms that the SRR2 enhancer regulates SOX2 expression in cancer. Full article
(This article belongs to the Special Issue The Role of SOX Transcription Factors in Cancer)
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20 pages, 4723 KiB  
Article
Targeting the Sonic Hedgehog Pathway to Suppress the Expression of the Cancer Stem Cell (CSC)—Related Transcription Factors and CSC-Driven Thyroid Tumor Growth
by Yurong Lu, Yiwen Zhu, Shihan Deng, Yuhuang Chen, Wei Li, Jing Sun and Xiulong Xu
Cancers 2021, 13(3), 418; https://doi.org/10.3390/cancers13030418 - 22 Jan 2021
Cited by 20 | Viewed by 2867
Abstract
The sonic hedgehog (Shh) pathway plays important roles in tumorigenesis, tumor growth, drug resistance, and metastasis. We and others have reported earlier that this pathway is highly activated in thyroid cancer. However, its role in thyroid cancer stem cell (CSC) self-renewal and tumor [...] Read more.
The sonic hedgehog (Shh) pathway plays important roles in tumorigenesis, tumor growth, drug resistance, and metastasis. We and others have reported earlier that this pathway is highly activated in thyroid cancer. However, its role in thyroid cancer stem cell (CSC) self-renewal and tumor development remains incompletely understood. B lymphoma Mo-MLV insertion region 1 homolog (BMI1) and SRY-Box Transcription Factor 2 (SOX2) are two CSC-related transcription factors that have been implicated in promoting CSC self-renewal. The objective of our current investigation was to determine the role of the Shh pathway in regulating BMI1 and SOX2 expression in thyroid cancer and promoting thyroid tumor growth and development. Here we report that inhibition of the Shh pathway by Gli1 siRNA or by cyclopamine and GANT61 reduced BMI1 and SOX2 expression in SW1736 and KAT-18 cells, two anaplastic thyroid cancer cell lines. The opposite results were obtained in cells overexpressing Gli1 or its downstream transcription factor Snail. The Shh pathway regulated SOX2 and BMI1 expression at a transcriptional and post-transcriptional level, respectively. GANT61 treatment suppressed the growth of SW1736 CSC-derived tumor xenografts but did not significantly inhibit the growth of tumors grown from bulk tumor cells. Clinicopathological analyses of thyroid tumor specimens by immunohistochemical (IHC) staining revealed that BMI1 and SOX2 were highly expressed in thyroid cancer and correlated with Gli1 expression. Our study provides evidence that activation of the Shh pathway leads to increased BMI1 and SOX2 expression in thyroid cancer and promotes thyroid CSC-driven tumor initiation. Targeting the Shh pathway may have therapeutic value for treating thyroid cancer and preventing recurrence. Full article
(This article belongs to the Special Issue The Role of SOX Transcription Factors in Cancer)
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