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Transcription Factors in Cancer Progression
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Transcription Factors in Cancer Progression

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 25977

Special Issue Editor

Dr. Behzad Mansoori

E-Mail Website
Guest Editor
Department of Cancer and Inflammation, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark
Interests: transcriptional factor; cancer; bioinformatic; immune system; miRNA; proliferation; drug resistance; cancer stem cells; DNA damage and repair; cell cycle; apoptosis; signaling transducers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Transcription factors (TFs) are proteins that control the rate of transcription of genetic information from DNA to messenger RNA, by binding to a specific DNA sequence. Studies showed TFs are commonly deregulated human malignancies. It was revealed that TFs are involved in cancer cell dependencies. Therefore, novel strategies such as gene silencing and CRISPR/Cas9 showed effective results for targeting TFs, highly effective in treating particular malignancies. Recently the role of TFs in cancer drug resistance attract scientific attention.

This Special Issue, entitled ‘Transcription Factors in Cancer Progression,’ invites research articles, reviews, and short communications including but not limited to: the mechanistic role of TFs and their regulatory networks, bioinformatic-based analysis of high-throughput clinical or cell line data in different datasets, TFs related to immune response, miRNA regulation on TFs, TFs in drug resistance, cancer stem cells, DNA damage and repair, proliferation, cell cycle, apoptosis, signalling transducers and comparative analysis which showed the networks between above mention functions.

Dr. Behzad Mansoori
Guest Editor

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. Genes is an international peer-reviewed open access monthly 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 2600 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

  • Transcriptional factor
  • Cancer
  • Bioinformatic
  • Immune system
  • miRNA
  • Proliferation
  • Drug resistance
  • cancer stem cells
  • DNA damage and repair
  • Cell cycle
  • Apoptosis
  • Signalling transducers

Published Papers (6 papers)

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Research

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18 pages, 3366 KiB  
Article
Silencing of HMGA2 by siRNA Loaded Methotrexate Functionalized Polyamidoamine Dendrimer for Human Breast Cancer Cell Therapy
by Fereydoon Abedi Gaballu, William Chi-Shing Cho, Gholamreza Dehghan, Amir Zarebkohan, Behzad Baradaran, Behzad Mansoori, Soheil Abbaspour-Ravasjani, Ali Mohammadi, Nader Sheibani, Ayuob Aghanejad and Jafar Ezzati Nazhad Dolatabadi
Genes 2021, 12(7), 1102; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12071102 - 20 Jul 2021
Cited by 14 | Viewed by 2848
Abstract
The transcription factor high mobility group protein A2 (HMGA2) plays an important role in the pathogenesis of some cancers including breast cancer. Polyamidoamine dendrimer generation 4 is a kind of highly branched polymeric nanoparticle with surface charge and highest density peripheral groups that [...] Read more.
The transcription factor high mobility group protein A2 (HMGA2) plays an important role in the pathogenesis of some cancers including breast cancer. Polyamidoamine dendrimer generation 4 is a kind of highly branched polymeric nanoparticle with surface charge and highest density peripheral groups that allow ligands or therapeutic agents to attach it, thereby facilitating target delivery. Here, methotrexate (MTX)- modified polyamidoamine dendrimer generation 4 (G4) (G4/MTX) was generated to deliver specific small interface RNA (siRNA) for suppressing HMGA2 expression and the consequent effects on folate receptor (FR) expressing human breast cancer cell lines (MCF-7, MDA-MB-231). We observed that HMGA2 siRNA was electrostatically adsorbed on the surface of the G4/MTX nanocarrier for constructing a G4/MTX-siRNA nano-complex which was verified by changing the final particle size and zeta potential. The release of MTX and siRNA from synthesized nanocomplexes was found in a time- and pH-dependent manner. We know that MTX targets FR. Interestingly, G4/MTX-siRNA demonstrates significant cellular internalization and gene silencing efficacy when compared to the control. Besides, the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay demonstrated selective cell cytotoxicity depending on the folate receptor expressing in a dose-dependent manner. The gene silencing and protein downregulation of HMGA2 by G4/MTX-siRNA was observed and could significantly induce cell apoptosis in MCF-7 and MDA-MB-231 cancer cells compared to the control group. Based on the findings, we suggest that the newly developed G4/MTX-siRNA nano-complex may be a promising strategy to increase apoptosis induction through HMGA2 suppression as a therapeutic target in human breast cancer. Full article
(This article belongs to the Special Issue Transcription Factors in Cancer Progression)
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17 pages, 3585 KiB  
Article
miR-34a and miR-200c Have an Additive Tumor-Suppressive Effect on Breast Cancer Cells and Patient Prognosis
by Behzad Mansoori, Nicola Silvestris, Ali Mohammadi, Vahid Khaze, Elham Baghbani, Ahad Mokhtarzadeh, Dariush Shanehbandi, Afshin Derakhshani, Pascal H. G. Duijf and Behzad Baradaran
Genes 2021, 12(2), 267; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12020267 - 12 Feb 2021
Cited by 26 | Viewed by 3144
Abstract
Breast cancer is the most common women’s malignancy in the world and, for subgroups of patients, treatment outcomes remain poor. Thus, more effective therapeutic strategies are urgently needed. MicroRNAs (miRNAs) have emerged as promising therapeutic tools and targets, as they play significant roles [...] Read more.
Breast cancer is the most common women’s malignancy in the world and, for subgroups of patients, treatment outcomes remain poor. Thus, more effective therapeutic strategies are urgently needed. MicroRNAs (miRNAs) have emerged as promising therapeutic tools and targets, as they play significant roles in regulating key cellular processes by suppressing gene expression. However, additive opportunities involving miRNAs have been underexplored. For example, both miR-34a and miR-200c individually suppress the development of different types of cancer, but the cellular effects of their combined actions remain unknown. Here, we show that miR-34a and miR-200c levels are reduced in breast tumors compared to adjacent normal tissues and that this additively predicts poor patient survival. In addition, in cell lines, miR-34a and miR-200c additively induce apoptosis and cell cycle arrest, while also inhibiting proliferation, invasion, migration, stemness and epithelial-to-mesenchymal transition (EMT). Mechanistically, both miRNA-34a and miR-200c directly target HIF1-α and subsequently downregulate VEGFR, MMP9 and CXCR4, although combined miRNA-34a and miR-200c delivery suppresses mouse xenograft tumor development as effectively as individual delivery. We establish a model, supported by in vitro and clinical data, which collectively suggest that the co-delivery of miR-34a and miR-200c represents a promising novel therapeutic strategy for breast cancer patients. Full article
(This article belongs to the Special Issue Transcription Factors in Cancer Progression)
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14 pages, 3983 KiB  
Article
Deregulated Immune Pathway Associated with Palbociclib Resistance in Preclinical Breast Cancer Models: Integrative Genomics and Transcriptomics
by Kamal Pandey, Eunbyeol Lee, Nahee Park, Jin Hur, Young Bin Cho, Nar Bahadur Katuwal, Seung Ki Kim, Seung Ah Lee, Isaac Kim, Hee Jung An, Sohyun Hwang and Yong Wha Moon
Genes 2021, 12(2), 159; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12020159 - 25 Jan 2021
Cited by 13 | Viewed by 3354
Abstract
Recently, cyclin-dependent kinase (CDK) 4/6 inhibitors have been widely used to treat advanced hormone receptor-positive breast cancer. Despite promising clinical outcomes, almost all patients eventually acquire resistance to CDK4/6 inhibitors. Here, we screened genes associated with palbociclib resistance through genomics and transcriptomics in [...] Read more.
Recently, cyclin-dependent kinase (CDK) 4/6 inhibitors have been widely used to treat advanced hormone receptor-positive breast cancer. Despite promising clinical outcomes, almost all patients eventually acquire resistance to CDK4/6 inhibitors. Here, we screened genes associated with palbociclib resistance through genomics and transcriptomics in preclinical breast cancer models. Palbociclib-resistant cells were generated by exposing hormone receptor-positive breast cancer cell lines to palbociclib. Whole-exome sequencing (WES) and a mRNA microarray were performed to compare the genomic and transcriptomic landscape between both palbociclib-sensitive and resistant cells. Microarray analysis revealed 651 differentially expressed genes (DEGs), while WES revealed 107 clinically significant mutated genes. Furthermore, pathway analysis of both DEGs and mutated genes revealed immune pathway deregulation in palbociclib-resistant cells. Notably, DEG annotation revealed activation of type I interferon pathway, activation of immune checkpoint inhibitory pathway, and suppression of immune checkpoint stimulatory pathway in palbociclib-resistant cells. Moreover, mutations in NCOR1, MUC4, and MUC16 genes found in palbociclib-resistant cells were annotated to be related to the immune pathway. In conclusion, our genomics and transcriptomics analysis using preclinical model, revealed that deregulated immune pathway is an additional mechanism of CDK4/6 inhibitor resistance besides the activation of cyclin E-CDK2 pathway and loss of RB, etc. Further studies are warranted to evaluate whether immune pathways may be a therapeutic target to overcome CDK4/6 inhibitor resistance. Full article
(This article belongs to the Special Issue Transcription Factors in Cancer Progression)
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Review

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19 pages, 2388 KiB  
Review
Long Non-Coding RNAs in Multidrug Resistance of Glioblastoma
by Parvaneh Mahinfar, Behzad Baradaran, Sadaf Davoudian, Fatemeh Vahidian, William Chi-Shing Cho and Behzad Mansoori
Genes 2021, 12(3), 455; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12030455 - 23 Mar 2021
Cited by 14 | Viewed by 3010
Abstract
Glioblastoma, also known as glioblastoma multiforme, is the most aggressive brain tumor in adults. Despite the huge advance in developing novel therapeutic strategies for patients with glioblastoma, the appearance of multidrug resistance (MDR) against the common chemotherapeutic agents, including temozolomide, is considered as [...] Read more.
Glioblastoma, also known as glioblastoma multiforme, is the most aggressive brain tumor in adults. Despite the huge advance in developing novel therapeutic strategies for patients with glioblastoma, the appearance of multidrug resistance (MDR) against the common chemotherapeutic agents, including temozolomide, is considered as one of the important causes for the failure of glioblastoma treatment. On the other hand, recent studies have demonstrated the critical roles of long non-coding RNAs (lncRNAs), particularly in the development of MDR in glioblastoma. Therefore, this article aimed to review lncRNA’s contribution to the regulation of MDR and elucidate the underlying mechanisms in glioblastoma, which will open up new lines of inquiry in the treatment of glioblastoma. Full article
(This article belongs to the Special Issue Transcription Factors in Cancer Progression)
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23 pages, 2058 KiB  
Review
HMGA2 as a Critical Regulator in Cancer Development
by Behzad Mansoori, Ali Mohammadi, Henrik J. Ditzel, Pascal H. G. Duijf, Vahid Khaze, Morten F. Gjerstorff and Behzad Baradaran
Genes 2021, 12(2), 269; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12020269 - 13 Feb 2021
Cited by 90 | Viewed by 9090
Abstract
The high mobility group protein 2 (HMGA2) regulates gene expression by binding to AT-rich regions of DNA. Akin to other DNA architectural proteins, HMGA2 is highly expressed in embryonic stem cells during embryogenesis, while its expression is more limited at later stages of [...] Read more.
The high mobility group protein 2 (HMGA2) regulates gene expression by binding to AT-rich regions of DNA. Akin to other DNA architectural proteins, HMGA2 is highly expressed in embryonic stem cells during embryogenesis, while its expression is more limited at later stages of development and in adulthood. Importantly, HMGA2 is re-expressed in nearly all human malignancies, where it promotes tumorigenesis by multiple mechanisms. HMGA2 increases cancer cell proliferation by promoting cell cycle entry and inhibition of apoptosis. In addition, HMGA2 influences different DNA repair mechanisms and promotes epithelial-to-mesenchymal transition by activating signaling via the MAPK/ERK, TGFβ/Smad, PI3K/AKT/mTOR, NFkB, and STAT3 pathways. Moreover, HMGA2 supports a cancer stem cell phenotype and renders cancer cells resistant to chemotherapeutic agents. In this review, we discuss these oncogenic roles of HMGA2 in different types of cancers and propose that HMGA2 may be used for cancer diagnostic, prognostic, and therapeutic purposes. Full article
(This article belongs to the Special Issue Transcription Factors in Cancer Progression)
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Other

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21 pages, 1276 KiB  
Systematic Review
A Systematic Review on the Therapeutic Potentiality of PD-L1-Inhibiting MicroRNAs for Triple-Negative Breast Cancer: Toward Single-Cell Sequencing-Guided Biomimetic Delivery
by Mahdi Abdoli Shadbad, Sahar Safaei, Oronzo Brunetti, Afshin Derakhshani, Parisa Lotfinejad, Ahad Mokhtarzadeh, Nima Hemmat, Vito Racanelli, Antonio Giovanni Solimando, Antonella Argentiero, Nicola Silvestris and Behzad Baradaran
Genes 2021, 12(8), 1206; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12081206 - 04 Aug 2021
Cited by 30 | Viewed by 3856
Abstract
The programmed death-ligand 1 (PD-L1)/programmed cell death protein 1 (PD-1) is a well-established inhibitory immune checkpoint axis in triple-negative breast cancer (TNBC). Growing evidence indicates that tumoral PD-L1 can lead to TNBC development. Although conventional immune checkpoint inhibitors have improved TNBC patients’ prognosis, [...] Read more.
The programmed death-ligand 1 (PD-L1)/programmed cell death protein 1 (PD-1) is a well-established inhibitory immune checkpoint axis in triple-negative breast cancer (TNBC). Growing evidence indicates that tumoral PD-L1 can lead to TNBC development. Although conventional immune checkpoint inhibitors have improved TNBC patients’ prognosis, their effect is mainly focused on improving anti-tumoral immune responses without substantially regulating oncogenic signaling pathways in tumoral cells. Moreover, the conventional immune checkpoint inhibitors cannot impede the de novo expression of oncoproteins, like PD-L1, in tumoral cells. Accumulating evidence has indicated that the restoration of specific microRNAs (miRs) can downregulate tumoral PD-L1 and inhibit TNBC development. Since miRs can target multiple mRNAs, miR-based gene therapy can be an appealing approach to inhibit the de novo expression of oncoproteins, like PD-L1, restore anti-tumoral immune responses, and regulate various intracellular singling pathways in TNBC. Therefore, we conducted the current systematic review based on the preferred reporting items for systematic reviews and meta-analyses (PRISMA) to provide a comprehensive and unbiased synthesis of currently available evidence regarding the effect of PD-L1-inhibiting miRs restoration on TNBC development and tumor microenvironment. For this purpose, we systematically searched the Cochrane Library, Embase, Scopus, PubMed, ProQuest, Web of Science, Ovid, and IranDoc databases to obtain the relevant peer-reviewed studies published before 25 May 2021. Based on the current evidence, the restoration of miR-424-5p, miR-138-5p, miR-570-3p, miR-200c-3p, miR-383-5p, miR-34a-5p, miR-3609, miR-195-5p, and miR-497-5p can inhibit tumoral PD-L1 expression, transform immunosuppressive tumor microenvironment into the pro-inflammatory tumor microenvironment, inhibit tumor proliferation, suppress tumor migration, enhance chemosensitivity of tumoral cells, stimulate tumor apoptosis, arrest cell cycle, repress the clonogenicity of tumoral cells, and regulate various oncogenic signaling pathways in TNBC cells. Concerning the biocompatibility of biomimetic carriers and the valuable insights provided by the single-cell sequencing technologies, single-cell sequencing-guided biomimetic delivery of these PD-L1-inhibiting miRs can decrease the toxicity of traditional approaches, increase the specificity of miR-delivery, enhance the efficacy of miR delivery, and provide the affected patients with personalized cancer therapy. Full article
(This article belongs to the Special Issue Transcription Factors in Cancer Progression)
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