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Cancer Cell Reprogramming 2.0

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

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 3139

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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
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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 the International Journal of Molecular Sciences, the focus will be on cancer stem cells, reprogramming cancer cells or malignant cancer cells to normal or benign tumor cells, or signaling pathways regulating cancer 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

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Published Papers (1 paper)

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Research

15 pages, 1599 KiB  
Article
MiR-125a-3p and MiR-320b Differentially Expressed in Patients with Chronic Myeloid Leukemia Treated with Allogeneic Hematopoietic Stem Cell Transplantation and Imatinib Mesylate
by Juliana R. B. Martins, Leonardo N. Moraes, Sarah S. Cury, Juliana Capannacci, Robson Francisco Carvalho, Célia Regina Nogueira, Newton Key Hokama and Paula O. M. Hokama
Int. J. Mol. Sci. 2021, 22(19), 10216; https://doi.org/10.3390/ijms221910216 - 23 Sep 2021
Cited by 5 | Viewed by 2508
Abstract
Chronic myeloid leukemia (CML), a hematopoietic neoplasm arising from the fusion of BCR (breakpoint cluster region) gene on chromosome 22 to the ABL (Abelson leukemia virus) gene on chromosome 9 (BCR-ABL1 oncogene), originates from a small population of leukemic stem cells with extensive [...] Read more.
Chronic myeloid leukemia (CML), a hematopoietic neoplasm arising from the fusion of BCR (breakpoint cluster region) gene on chromosome 22 to the ABL (Abelson leukemia virus) gene on chromosome 9 (BCR-ABL1 oncogene), originates from a small population of leukemic stem cells with extensive capacity for self-renewal and an inflammatory microenvironment. Currently, CML treatment is based on tyrosine kinase inhibitors (TKIs). However, allogeneic hematopoietic stem cell transplantation (HSCT-allo) is currently the only effective treatment of CML. The difficulty of finding a compatible donor and high rates of morbidity and mortality limit transplantation treatment. Despite the safety and efficacy of TKIs, patients can develop resistance. Thus, microRNAs (miRNAs) play a prominent role as biomarkers and post-transcriptional regulators of gene expression. The aim of this study was to analyze the miRNA profile in CML patients who achieved cytogenetic remission after treatment with both HSCT-allo and TKI. Expression analyses of the 758 miRNAs were performed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Bioinformatics tools were used for data analysis. We detected miRNA profiles using their possible target genes and target pathways. MiR-125a-3p stood out among the downregulated miRNAs, showing an interaction network with 52 target genes. MiR-320b was the only upregulated miRNA, with an interaction network of 26 genes. The results are expected to aid future studies of miRNAs, residual leukemic cells, and prognosis in CML. Full article
(This article belongs to the Special Issue Cancer Cell Reprogramming 2.0)
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