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Gene Networks That Control Cell Proliferation and Differentiation
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Gene Networks That Control Cell Proliferation and Differentiation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 9768

Special Issue Editor

Prof. Dr. Bhagwati Gupta

E-Mail Website1 Website2
Guest Editor
Faculty of Science, McMaster University, Hamilton, ON, Canada
Interests: developmental genetics; molecular biology; molecular genetics; genomics; disease models; cell signaling; organ formation; neurobiology; gene networks; cell proliferation and differentiation; evolution of developmental mechanisms

Special Issue Information

Dear Colleagues,

Cell proliferation and differentiation are fundamental processes in multicellular eukaryotes. The regulation of these events is not only crucial to generate the desired number and diversity of cells during development, but also throughout life for processes such as tissue repair. Research in animal models has led to the discovery of a large number of genes that function to control cell division, and these cells ultimately differentiate to form different parts of the body. Many of the identified genes are shown to form regulatory networks and encode components of evolutionarily conserved signal transduction pathways. Functional studies have revealed that alterations in gene regulation and pathway activities can affect the ability of cells to divide and differentiate, which could cause diseases and lead to premature death of the animal. Hence, a comprehensive understanding of gene interactions and regulatory networks is needed to advance biomedical discoveries to treat illnesses. The Special Issue “Gene Networks That Control Cell Proliferation and Differentiation” of the International Journal of Molecular Sciences will include original research articles and reviews describing molecular mechanisms of processes in both normal and disease contexts. Studies using a wide range of genetic, cell biological, molecular, genome-wide, and bioinformatic approaches are encouraged.

Prof. Dr. Bhagwati Gupta
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Cell proliferation
  • Cell differentiation
  • Gene function
  • Gene network
  • Signaling

Published Papers (4 papers)

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Research

18 pages, 2327 KiB  
Article
Generation and Characterization of Human Mesenchymal Stem Cell-Derived Smooth Muscle Cells
by Srikanth Sivaraman, Jackson Hedrick, Samia Ismail, Chris Slavin and Raj R. Rao
Int. J. Mol. Sci. 2021, 22(19), 10335; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910335 - 25 Sep 2021
Cited by 5 | Viewed by 2292
Abstract
Cardiovascular diseases are the leading cause of death worldwide. A completely autologous treatment can be achieved by using elastogenic mesenchymal stem cell (MSC)-derived smooth muscle cells (SMC) at the affected tissue site of vascular diseases such as abdominal aortic aneurysms (AAA). Thus, our [...] Read more.
Cardiovascular diseases are the leading cause of death worldwide. A completely autologous treatment can be achieved by using elastogenic mesenchymal stem cell (MSC)-derived smooth muscle cells (SMC) at the affected tissue site of vascular diseases such as abdominal aortic aneurysms (AAA). Thus, our work focused on evaluating the efficacy of (a) the combination of various growth factors, (b) different time periods and (c) different MSC lines to determine the treatment combination that generated SMCs that exhibited the greatest elastogenicity among the tested groups using Western blotting and flow cytometry. Additionally, total RNA sequencing was used to confirm that post-differentiation cells were upregulating SMC-specific gene markers. Results indicated that MSCs cultured for four days in PDGF + TGFβ1 (PT)-infused differentiation medium showed significant increases in SMC markers and decreases in MSC markers compared to MSCs cultured without differentiation factors. RNA Seq analysis confirmed the presence of vascular smooth muscle formation in MSCs differentiated in PT medium over a seven-day period. Overall, our results indicated that origin, growth factor treatment and culture period played a major role in influencing MSC differentiation to SMCs. Full article
(This article belongs to the Special Issue Gene Networks That Control Cell Proliferation and Differentiation)
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12 pages, 3510 KiB  
Article
Cultivation of Head and Neck Squamous Cell Carcinoma Cells with Wound Fluid Leads to Cisplatin Resistance via Epithelial-Mesenchymal Transition Induction
by Till Jasper Meyer, Manuel Stöth, Helena Moratin, Pascal Ickrath, Marietta Herrmann, Norbert Kleinsasser, Rudolf Hagen, Stephan Hackenberg and Agmal Scherzad
Int. J. Mol. Sci. 2021, 22(9), 4474; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094474 - 25 Apr 2021
Cited by 2 | Viewed by 1786
Abstract
Locoregional recurrence is a major reason for therapy failure after surgical resection of head and neck squamous cell carcinoma (HNSCC). The physiological process of postoperative wound healing could potentially support the proliferation of remaining tumor cells. The aim of this study was to [...] Read more.
Locoregional recurrence is a major reason for therapy failure after surgical resection of head and neck squamous cell carcinoma (HNSCC). The physiological process of postoperative wound healing could potentially support the proliferation of remaining tumor cells. The aim of this study was to evaluate the influence of wound fluid (WF) on the cell cycle distribution and a potential induction of epithelial-mesenchymal transition (EMT). To verify this hypothesis, we incubated FaDu and HLaC78 cells with postoperative WF from patients after neck dissection. Cell viability in dependence of WF concentration and cisplatin was measured by flow cytometry. Cell cycle analysis was performed by flow cytometry and EMT-marker expression by rtPCR. WF showed high concentrations of interleukin (IL)-6, IL-8, IL-10, CCL2, MCP-1, EGF, angiogenin, and leptin. The cultivation of tumor cells with WF resulted in a significant increase in cell proliferation without affecting the cell cycle. In addition, there was a significant enhancement of the mesenchymal markers Snail 2 and vimentin, while the expression of the epithelial marker E-cadherin was significantly decreased. After cisplatin treatment, tumor cells incubated with WF showed a significantly higher resistance compared with the control group. The effect of cisplatin-resistance was dependent on the WF concentration. In summary, proinflammatory cytokines are predominantly found in WF. Furthermore, the results suggest that EMT can be induced by WF, which could be a possible mechanism for cisplatin resistance. Full article
(This article belongs to the Special Issue Gene Networks That Control Cell Proliferation and Differentiation)
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18 pages, 7197 KiB  
Article
Overexpression of miR-1306-5p, miR-3195, and miR-3914 Inhibits Ameloblast Differentiation through Suppression of Genes Associated with Human Amelogenesis Imperfecta
by Hiroki Yoshioka, Yin-Ying Wang, Akiko Suzuki, Meysam Shayegh, Mona V. Gajera, Zhongming Zhao and Junichi Iwata
Int. J. Mol. Sci. 2021, 22(4), 2202; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042202 - 23 Feb 2021
Cited by 9 | Viewed by 2577
Abstract
Amelogenesis imperfecta is a congenital form of enamel hypoplasia. Although a number of genetic mutations have been reported in humans, the regulatory network of these genes remains mostly unclear. To identify signatures of biological pathways in amelogenesis imperfecta, we conducted bioinformatic analyses on [...] Read more.
Amelogenesis imperfecta is a congenital form of enamel hypoplasia. Although a number of genetic mutations have been reported in humans, the regulatory network of these genes remains mostly unclear. To identify signatures of biological pathways in amelogenesis imperfecta, we conducted bioinformatic analyses on genes associated with the condition in humans. Through an extensive search of the main biomedical databases, we found 56 genes in which mutations and/or association/linkage were reported in individuals with amelogenesis imperfecta. These candidate genes were further grouped by function, pathway, protein–protein interaction, and tissue-specific expression patterns using various bioinformatic tools. The bioinformatic analyses highlighted a group of genes essential for extracellular matrix formation. Furthermore, advanced bioinformatic analyses for microRNAs (miRNAs), which are short non-coding RNAs that suppress target genes at the post-transcriptional level, predicted 37 candidates that may be involved in amelogenesis imperfecta. To validate the miRNA–gene regulation association, we analyzed the target gene expression of the top seven candidate miRNAs: miR-3195, miR-382-5p, miR-1306-5p, miR-4683, miR-6716-3p, miR-3914, and miR-3935. Among them, miR-1306-5p, miR-3195, and miR-3914 were confirmed to regulate ameloblast differentiation through the regulation of genes associated with amelogenesis imperfecta in AM-1 cells, a human ameloblastoma cell line. Taken together, our study suggests a potential role for miRNAs in amelogenesis imperfecta. Full article
(This article belongs to the Special Issue Gene Networks That Control Cell Proliferation and Differentiation)
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15 pages, 2670 KiB  
Article
Developmental Roles of FUSE Binding Protein 1 (Fubp1) in Tooth Morphogenesis
by Yam Prasad Aryal, Sanjiv Neupane, Tae-Young Kim, Eui-Seon Lee, Nitin Kumar Pokhrel, Chang-Yeol Yeon, Ji-Youn Kim, Chang-Hyeon An, Seo-Young An, Eui-Kyun Park, Jung-Hong Ha, Jae-Kwang Jung, Hitoshi Yamamoto, Sung-Won Cho, Sanggyu Lee, Do-Yeon Kim, Tae-Yub Kwon, Youngkyun Lee, Wern-Joo Sohn and Jae-Young Kim
Int. J. Mol. Sci. 2020, 21(21), 8079; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218079 - 29 Oct 2020
Cited by 5 | Viewed by 2479
Abstract
FUSE binding protein 1 (Fubp1), a regulator of the c-Myc transcription factor and a DNA/RNA-binding protein, plays important roles in the regulation of gene transcription and cellular physiology. In this study, to reveal the precise developmental function of Fubp1, we [...] Read more.
FUSE binding protein 1 (Fubp1), a regulator of the c-Myc transcription factor and a DNA/RNA-binding protein, plays important roles in the regulation of gene transcription and cellular physiology. In this study, to reveal the precise developmental function of Fubp1, we examined the detailed expression pattern and developmental function of Fubp1 during tooth morphogenesis by RT-qPCR, in situ hybridization, and knock-down study using in vitro organ cultivation methods. In embryogenesis, Fubp1 is obviously expressed in the enamel organ and condensed mesenchyme, known to be important for proper tooth formation. Knocking down Fubp1 at E14 for two days, showed the altered expression patterns of tooth development related signalling molecules, including Bmps and Fgf4. In addition, transient knock-down of Fubp1 at E14 revealed changes in the localization patterns of c-Myc and cell proliferation in epithelium and mesenchyme, related with altered tooth morphogenesis. These results also showed the decreased amelogenin and dentin sialophosphoprotein expressions and disrupted enamel rod and interrod formation in one- and three-week renal transplanted teeth respectively. Thus, our results suggested that Fubp1 plays a modulating role during dentinogenesis and amelogenesis by regulating the expression pattern of signalling molecules to achieve the proper structural formation of hard tissue matrices and crown morphogenesis in mice molar development. Full article
(This article belongs to the Special Issue Gene Networks That Control Cell Proliferation and Differentiation)
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