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Cell Reprogramming
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Cell Reprogramming

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

Deadline for manuscript submissions: closed (28 February 2018) | Viewed by 32450

Special Issue Editor

Prof. Dr. Ssang-Goo Cho

E-Mail Website
Guest Editor
Department of Stem Cell and Regenerative Biology, Konkuk University, Seoul, Republic of Korea
Interests: transplantation; signaling pathways in stem, cancer, and cancer stem cells; molecular mechanism of cellular reprogramming; apoptosis and autophagy; cancer stem cells; induced pluripotent stem cells; pancreatic beta-cell differentiation; pancreatic cancer cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Stem cells are defined as cells that have the capacity to perpetuate themselves through self-renewal and to generate mature cells of a specific tissue through differentiation. They are considered to be a promising tool for the treatment of patients experiencing serious degenerative and incurable diseases. Recently, there has been a significant turning point in the field of stem cells after the development of induced pluripotent stem cells (iPS cells) technology. Reprogramming of somatic cells is the hallmark of this technology, and also it can be derived for adult tissues, as well as from the patients’ tissue. Of note, iPS cells technology may overcome the hurdle of moral and ethical issues that arise from using human ES cells, as well as immune rejection. Cancer research also developed a new turn due to iPSC technology. The reprogramming of cancer cells is an interesting approach to the study of cancer-related genes and the interaction between these genes and the cellular microenvironment, before and after reprogramming, to explain the mechanisms of various stages of cancer development. Cancer cell reprogramming may be one of the ways to develop novel cancer treatments, as cancer cells may be converted into an immature or benign state. As normal stem cells and cancer cells share the capacity to self-renew, it seems reasonable to propose that newly-arising cancer cells appropriate the machinery for self-renewing cell division, which is normally expressed in stem cells. Evidence shows that many pathways that are classically associated with cancer may also regulate normal stem cell development. Signaling pathways associated with oncogenesis, metastasis, epithelial–mesenchymal transition (EMT), or mesenchymal–epithelial transition (MET), such as the Notch, Sonic hedgehog (Shh), Wnt, kinase, GPCR signaling pathways, may also regulate stem cell self-renewal.

In this Special Issue of IJMS, the focus will be on reprogramming somatic cells to stem cells or cancer stem cells, Reprogramming cancer cells or malignant cancer cells to normal or benign tumor cells, or signaling pathways regulating stem cell self-renewal or oncogenesis metastasis, epithelial–mesenchymal transition (EMT), or mesenchymal–epithelial transition (MET) in relation to new treatment options or other biological and medical applications.

Prof. Dr. Ssang-Goo Cho
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 reprogramming of somatic cells
  • stem cells
  • cancer stem cells
  • Reprogramming of cancer cells
  • malignant cancer cells
  • normal or benign tumor cells
  • signaling pathways regulating stem cell self-renewal and oncogenesis
  • self-renewal
  • oncogenesis
  • metastasis
  • epithelial–mesenchymal transition (EMT)
  • mesenchymal– epithelial transition (MET)EMT/MET

Related Special Issue

Published Papers (5 papers)

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Research

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21 pages, 4388 KiB  
Article
Cytokeratin 19 (KRT19) has a Role in the Reprogramming of Cancer Stem Cell-Like Cells to Less Aggressive and More Drug-Sensitive Cells
by Subbroto Kumar Saha, Kyeongseok Kim, Gwang-Mo Yang, Hye Yeon Choi and Ssang-Goo Cho
Int. J. Mol. Sci. 2018, 19(5), 1423; https://doi.org/10.3390/ijms19051423 - 09 May 2018
Cited by 33 | Viewed by 7247
Abstract
Cytokeratin 19 (KRT19) is a cytoplasmic intermediate filament protein, which is responsible for structural rigidity and multipurpose scaffolds. In several cancers, KRT19 is overexpressed and may play a crucial role in tumorigenic transformation. In our previous study, we revealed the role [...] Read more.
Cytokeratin 19 (KRT19) is a cytoplasmic intermediate filament protein, which is responsible for structural rigidity and multipurpose scaffolds. In several cancers, KRT19 is overexpressed and may play a crucial role in tumorigenic transformation. In our previous study, we revealed the role of KRT19 as signaling component which mediated Wnt/NOTCH crosstalk through NUMB transcription in breast cancer. Here, we investigated the function of KRT19 in cancer reprogramming and drug resistance in breast cancer cells. We found that expression of KRT19 was attenuated in several patients-derived breast cancer tissues and patients with a low expression of KRT19 were significantly correlated with poor prognosis in breast cancer patients. Consistently, highly aggressive and drug-resistant breast cancer patient-derived cancer stem cell-like cells (konkuk university-cancer stem cell-like cell (KU-CSLCs)) displayed higher expression of cancer stem cell (CSC) markers, including ALDH1, CXCR4, and CD133, but a much lower expression of KRT19 than that is seen in highly aggressive triple negative breast cancer MDA-MB231 cells. Moreover, we revealed that the knockdown of KRT19 in MDA-MB231 cells led to an enhancement of cancer properties, such as cell proliferation, sphere formation, migration, and drug resistance, while the overexpression of KRT19 in KU-CSLCs resulted in the significant attenuation of cancer properties. KRT19 regulated cancer stem cell reprogramming by modulating the expression of cancer stem cell markers (ALDH1, CXCR4, and CD133), as well as the phosphorylation of Src and GSK3β (Tyr216). Therefore, our data may imply that the modulation of KRT19 expression could be involved in cancer stem cell reprogramming and drug sensitivity, which might have clinical implications for cancer or cancer stem cell treatment. Full article
(This article belongs to the Special Issue Cell Reprogramming)
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14 pages, 13966 KiB  
Article
S-phase Synchronization Facilitates the Early Progression of Induced-Cardiomyocyte Reprogramming through Enhanced Cell-Cycle Exit
by Emre Bektik, Adrienne Dennis, Gary Pawlowski, Chen Zhou, Danielle Maleski, Satoru Takahashi, Kenneth R. Laurita, Isabelle Deschênes and Ji-Dong Fu
Int. J. Mol. Sci. 2018, 19(5), 1364; https://doi.org/10.3390/ijms19051364 - 04 May 2018
Cited by 15 | Viewed by 4808
Abstract
Direct reprogramming of fibroblasts into induced cardiomyocytes (iCMs) holds a great promise for regenerative medicine and has been studied in several major directions. However, cell-cycle regulation, a fundamental biological process, has not been investigated during iCM-reprogramming. Here, our time-lapse imaging on iCMs, reprogrammed [...] Read more.
Direct reprogramming of fibroblasts into induced cardiomyocytes (iCMs) holds a great promise for regenerative medicine and has been studied in several major directions. However, cell-cycle regulation, a fundamental biological process, has not been investigated during iCM-reprogramming. Here, our time-lapse imaging on iCMs, reprogrammed by Gata4, Mef2c, and Tbx5 (GMT) monocistronic retroviruses, revealed that iCM-reprogramming was majorly initiated at late-G1- or S-phase and nearly half of GMT-reprogrammed iCMs divided soon after reprogramming. iCMs exited cell cycle along the process of reprogramming with decreased percentage of 5-ethynyl-20-deoxyuridine (EdU)+/α-myosin heavy chain (αMHC)-GFP+ cells. S-phase synchronization post-GMT-infection could enhance cell-cycle exit of reprogrammed iCMs and yield more GFPhigh iCMs, which achieved an advanced reprogramming with more expression of cardiac genes than GFPlow cells. However, S-phase synchronization did not enhance the reprogramming with a polycistronic-viral vector, in which cell-cycle exit had been accelerated. In conclusion, post-infection synchronization of S-phase facilitated the early progression of GMT-reprogramming through a mechanism of enhanced cell-cycle exit. Full article
(This article belongs to the Special Issue Cell Reprogramming)
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14 pages, 3626 KiB  
Article
Lipid Supplement in the Cultural Condition Facilitates the Porcine iPSC Derivation through cAMP/PKA/CREB Signal Pathway
by Wei Zhang, Hanning Wang, Shaopeng Zhang, Liang Zhong, Yanliang Wang, Yangli Pei, Jianyong Han and Suying Cao
Int. J. Mol. Sci. 2018, 19(2), 509; https://doi.org/10.3390/ijms19020509 - 08 Feb 2018
Cited by 15 | Viewed by 6156
Abstract
Large numbers of lipids exist in the porcine oocytes and early embryos and have the positive effects on their development, suggesting that the lipids may play an important role in pluripotency establishment and maintenance in pigs. However, the effects of lipids and their [...] Read more.
Large numbers of lipids exist in the porcine oocytes and early embryos and have the positive effects on their development, suggesting that the lipids may play an important role in pluripotency establishment and maintenance in pigs. However, the effects of lipids and their metabolites, such as fatty acids on reprogramming and the pluripotency gene expression of porcine-induced pluripotent stem cells (iPSCs), are unclear. Here, we generated the porcine iPSCs that resemble the mouse embryonic stem cells (ESCs) under lipid and fatty-acid-enriched cultural conditions (supplement of AlbuMAX). These porcine iPSCs show positive for the ESCs pluripotency markers and have the differentiation abilities to all three germ layers, and importantly, have the capability of aggregation into the inner cell mass (ICM) of porcine blastocysts. We further confirmed that lipid and fatty acid enriched condition can promote the cell proliferation and improve reprogramming efficiency by elevating cAMP levels. Interestingly, this lipids supplement promotes mesenchymal–epithelial transition (MET) through the cAMP/PKA/CREB signal pathway and upregulates the E-cadherin expression during porcine somatic cell reprogramming. The lipids supplement also makes a contribution to lipid droplets accumulation in the porcine iPSCs that resemble porcine preimplantation embryos. These findings may facilitate understanding of the lipid metabolism in porcine iPSCs and lay the foundation of bona fide porcine embryonic stem cell derivation. Full article
(This article belongs to the Special Issue Cell Reprogramming)
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Review

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11 pages, 326 KiB  
Review
Induced Tissue-Specific Stem Cells and Epigenetic Memory in Induced Pluripotent Stem Cells
by Hirofumi Noguchi, Chika Miyagi-Shiohira and Yoshiki Nakashima
Int. J. Mol. Sci. 2018, 19(4), 930; https://doi.org/10.3390/ijms19040930 - 21 Mar 2018
Cited by 44 | Viewed by 7016
Abstract
Induced pluripotent stem (iPS) cells have significant implications for overcoming most of the ethical issues associated with embryonic stem (ES) cells. The pattern of expressed genes, DNA methylation, and covalent histone modifications in iPS cells are very similar to those in ES cells. [...] Read more.
Induced pluripotent stem (iPS) cells have significant implications for overcoming most of the ethical issues associated with embryonic stem (ES) cells. The pattern of expressed genes, DNA methylation, and covalent histone modifications in iPS cells are very similar to those in ES cells. However, it has recently been shown that, following the reprogramming of mouse/human iPS cells, epigenetic memory is inherited from the parental cells. These findings suggest that the phenotype of iPS cells may be influenced by their cells of origin and that their skewed differentiation potential may prove useful in the generation of differentiated cell types that are currently difficult to produce from ES/iPS cells for the treatment of human diseases. Our recent study demonstrated the generation of induced tissue-specific stem (iTS) cells by transient overexpression of the reprogramming factors combined with tissue-specific selection. iTS cells are cells that inherit numerous components of epigenetic memory from donor tissue and acquire self-renewal potential. This review describes the “epigenetic memory” phenomenon in iPS and iTS cells and the possible clinical applications of these stem cells. Full article
(This article belongs to the Special Issue Cell Reprogramming)
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31 pages, 1359 KiB  
Review
Expansion of Sphingosine Kinase and Sphingosine-1-Phosphate Receptor Function in Normal and Cancer Cells: From Membrane Restructuring to Mediation of Estrogen Signaling and Stem Cell Programming
by Olga A. Sukocheva
Int. J. Mol. Sci. 2018, 19(2), 420; https://doi.org/10.3390/ijms19020420 - 31 Jan 2018
Cited by 49 | Viewed by 6589
Abstract
Sphingolipids, sphingolipid metabolizing enzymes, and their receptors network are being recognized as part of the signaling mechanisms, which govern breast cancer cell growth, migration, and survival during chemotherapy treatment. Approximately 70% of breast cancers are estrogen receptor (ER) positive and, thus, rely on [...] Read more.
Sphingolipids, sphingolipid metabolizing enzymes, and their receptors network are being recognized as part of the signaling mechanisms, which govern breast cancer cell growth, migration, and survival during chemotherapy treatment. Approximately 70% of breast cancers are estrogen receptor (ER) positive and, thus, rely on estrogen signaling. Estrogen activates an intracellular network composed of many cytoplasmic and nuclear mediators. Some estrogen effects can be mediated by sphingolipids. Estrogen activates sphingosine kinase 1 (SphK1) and amplifies the intracellular concentration of sphingosine-1-phosphate (S1P) in breast cancer cells during stimulation of proliferation and survival. Specifically, Estrogen activates S1P receptors (S1PR) and induces growth factor receptor transactivation. SphK, S1P, and S1PR expression are causally associated with endocrine resistance and progression to advanced tumor stages in ER-positive breast cancers in vivo. Recently, the network of SphK/S1PR was shown to promote the development of ER-negative cancers and breast cancer stem cells, as well as stimulating angiogenesis. Novel findings confirm and broaden our knowledge about the cross-talk between sphingolipids and estrogen network in normal and malignant cells. Current S1PRs therapeutic inhibition was indicated as a promising chemotherapy approach in non-responsive and advanced malignancies. Considering that sphingolipid signaling has a prominent role in terminally differentiated cells, the impact should be considered when designing specific SphK/S1PR inhibitors. This study analyzes the dynamic of the transformation of sphingolipid axis during a transition from normal to pathological condition on the level of the whole organism. The sphingolipid-based mediation and facilitation of global effects of estrogen were critically accented as a bridging mechanism that should be explored in cancer prevention. Full article
(This article belongs to the Special Issue Cell Reprogramming)
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