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Cancer Cell Reprogramming
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Cancer Cell Reprogramming

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 (30 June 2020) | Viewed by 24158

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 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

Manuscript Submission Information

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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.

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Related Special Issue

Published Papers (6 papers)

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Research

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19 pages, 3436 KiB  
Article
IKKβ Kinase Promotes Stemness, Migration, and Invasion in KRAS-Driven Lung Adenocarcinoma Cells
by Felipe Silva Rodrigues, Vanessa Silva Miranda, Tatiana Correa Carneiro-Lobo, Luiza Coimbra Scalabrini, Björn Kruspig, Elena Levantini, Daniel J. Murphy and Daniela Sanchez Bassères
Int. J. Mol. Sci. 2020, 21(16), 5806; https://doi.org/10.3390/ijms21165806 - 13 Aug 2020
Cited by 1 | Viewed by 3593
Abstract
KRAS oncogenic mutations are widespread in lung cancer and, because direct targeting of KRAS has proven to be challenging, KRAS-driven cancers lack effective therapies. One alternative strategy for developing KRAS targeted therapies is to identify downstream targets involved in promoting important malignant features, [...] Read more.
KRAS oncogenic mutations are widespread in lung cancer and, because direct targeting of KRAS has proven to be challenging, KRAS-driven cancers lack effective therapies. One alternative strategy for developing KRAS targeted therapies is to identify downstream targets involved in promoting important malignant features, such as the acquisition of a cancer stem-like and metastatic phenotype. Based on previous studies showing that KRAS activates nuclear factor kappa-B (NF-κB) through inhibitor of nuclear factor kappa-B kinase β (IKKβ) to promote lung tumourigenesis, we hypothesized that inhibition of IKKβ would reduce stemness, migration and invasion of KRAS-mutant human lung cancer cells. We show that KRAS-driven lung tumoursphere-derived cells exhibit stemness features and increased IKKβ kinase activity. IKKβ targeting by different approaches reduces the expression of stemness-associated genes, tumoursphere formation, and self-renewal, and preferentially impairs the proliferation of KRAS-driven lung tumoursphere-derived cells. Moreover, we show that IKKβ targeting reduces tumour cell migration and invasion, potentially by regulating both expression and activity of matrix metalloproteinase 2 (MMP2). In conclusion, our results indicate that IKKβ is an important mediator of KRAS-induced stemness and invasive features in lung cancer, and, therefore, might constitute a promising strategy to lower recurrence rates, reduce metastatic dissemination, and improve survival of lung cancer patients with KRAS-driven disease. Full article
(This article belongs to the Special Issue Cancer Cell Reprogramming)
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14 pages, 3589 KiB  
Article
Underlying Ossification Phenotype in a Murine Model of Metastatic Synovial Sarcoma
by Matthew Kirkham, Austen Kalivas, Kaniz Fatema, Sarah Luelling, Brooke H. Dubansky, Benjamin Dubansky, Kevin B. Jones and Jared J. Barrott
Int. J. Mol. Sci. 2020, 21(7), 2636; https://doi.org/10.3390/ijms21072636 - 10 Apr 2020
Cited by 2 | Viewed by 3382
Abstract
Synovial sarcoma, an uncommon cancer, typically affects young adults. Survival rates range from 36% to 76%, decreasing significantly when metastases are present. Synovial sarcomas form in soft tissues, often near bones, with about 10% demonstrating ossification in the tumor. The literature is inconclusive [...] Read more.
Synovial sarcoma, an uncommon cancer, typically affects young adults. Survival rates range from 36% to 76%, decreasing significantly when metastases are present. Synovial sarcomas form in soft tissues, often near bones, with about 10% demonstrating ossification in the tumor. The literature is inconclusive on whether the presence of ossification portends a worse prognosis. To this end, we analyzed our genetic mouse models of synovial sarcoma to determine the extent of ossification in the tumors and its relationship with morbidity. We noted higher ossification within our metastatic mouse model of synovial sarcoma. Not only did we observe ossification within the tumors at a frequency of 7%, but an even higher frequency, 72%, of bone reactivity was detected by radiography. An enrichment of bone development genes was associated with primary tumors, even in the absence of an ossification phenotype. In spite of the ossification being intricately linked with the metastatic model, the presence of ossification was not associated with a faster or worse morbidity in the mice. Our conclusion is that both metastasis and ossification are dependent on time, but that they are independent of one another. Full article
(This article belongs to the Special Issue Cancer Cell Reprogramming)
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15 pages, 2855 KiB  
Article
Differential Expression Profiles of Oxidative Stress Levels, 8-oxo-dG and 4-HNE, in Barrett’s Esophagus Compared to Esophageal Adenocarcinoma
by Naoimh J. O’Farrell, James J. Phelan, Ronan Feighery, Brendan Doyle, Sarah L. Picardo, Narayanasamy Ravi, Dermot O’Toole, John V. Reynolds and Jacintha O’Sullivan
Int. J. Mol. Sci. 2019, 20(18), 4449; https://doi.org/10.3390/ijms20184449 - 10 Sep 2019
Cited by 20 | Viewed by 3170
Abstract
Barrett’s esophagus (BE), a chronic inflammatory condition, is the leading risk factor for esophageal adenocarcinoma (EAC). In inflammation to cancer pathways, oxidative stress profiles have been linked to cancer progression. However, the relevance of oxidative stress profiles along the BE-disease sequence remains to [...] Read more.
Barrett’s esophagus (BE), a chronic inflammatory condition, is the leading risk factor for esophageal adenocarcinoma (EAC). In inflammation to cancer pathways, oxidative stress profiles have been linked to cancer progression. However, the relevance of oxidative stress profiles along the BE-disease sequence remains to be elucidated. In this study, markers of oxidative stress; DNA adducts (8-oxo-dG) and lipoperoxidation (4-HNE), and markers of proliferation (Ki67) were measured in patient biopsies representing the BE-disease sequence. Differences in expression of these markers in Barrett’s patients with cancer-progression and non-progression were examined. Proliferation was reduced in Barrett’s specialized intestinal metaplasia (SIM) compared with EAC (p < 0.035). Correcting for cell proliferation levels, a confounding factor, linked to oxidative stress profiles, SIM demonstrated increased levels of 8-oxo-dG and 4-HNE (p < 0.05) compared with EAC. Longitudinal analysis of Barrett’s patients demonstrated decreased levels of 8-oxo-dG in SIM cancer progression (p < 0.05). BE is an environment of increased oxidative stress and inflammation. Patients with progressive disease demonstrated reduced oxidative stress levels in 8-oxo-dG. Perhaps these alterations facilitate Barrett’s progression, whereas in non-progressive disease, cells follow the rules of increased oxidative stress ultimately triggers cell apoptosis, thereby preventing propagation and survival. Full article
(This article belongs to the Special Issue Cancer Cell Reprogramming)
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11 pages, 2659 KiB  
Article
A Soft Matrix Enhances the Cancer Stem Cell Phenotype of HCC Cells
by Boren Tian, Qing Luo, Yang Ju and Guanbin Song
Int. J. Mol. Sci. 2019, 20(11), 2831; https://doi.org/10.3390/ijms20112831 - 10 Jun 2019
Cited by 40 | Viewed by 4184
Abstract
Cancer stem cells (CSCs) comprise a small portion of cancer cells, have greater self-renewal ability and metastatic potential than non-CSCs and are resistant to drugs and radiotherapy. CSCs and non-CSCs, which can reversibly change their stemness states, typically play roles in plasticity and [...] Read more.
Cancer stem cells (CSCs) comprise a small portion of cancer cells, have greater self-renewal ability and metastatic potential than non-CSCs and are resistant to drugs and radiotherapy. CSCs and non-CSCs, which can reversibly change their stemness states, typically play roles in plasticity and cancer cell heterogeneity. Furthermore, the component that plays a key role in affecting CSC plasticity remains unknown. In this study, we utilized mechanically tunable polyacrylamide (PA) hydrogels to simulate different stiffnesses of the liver tissue matrix in various stages. Our results showed that hepatocellular carcinoma (HCC) cells were small and round in a soft matrix. The soft matrix increased the expression levels of liver cancer cells with stemness properties (LCSC) surface markers in HCC cells and the number of side population (SP) cells. Moreover, the soft matrix elicited early cell cycle arrest in the G1 phase and increased the cell sphere-forming ability. In addition, cells grown on the soft matrix showed enhanced chemoresistance and tumorigenicity potential. In summary, our study demonstrated that a soft matrix increases the stemness of HCC cells. Full article
(This article belongs to the Special Issue Cancer Cell Reprogramming)
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13 pages, 2886 KiB  
Article
The Root Bark of Morus alba L. Suppressed the Migration of Human Non-Small-Cell Lung Cancer Cells through Inhibition of Epithelial–Mesenchymal Transition Mediated by STAT3 and Src
by Tae-Rin Min, Hyun-Ji Park, Moon Nyeo Park, Bonglee Kim and Shin-Hyung Park
Int. J. Mol. Sci. 2019, 20(9), 2244; https://doi.org/10.3390/ijms20092244 - 07 May 2019
Cited by 27 | Viewed by 3449
Abstract
The root bark of Morus alba L. (MA) has been traditionally used for the treatment of various lung diseases in Korea. Although recent research has demonstrated its anticancer effects in several cancer cells, it is still unclear whether MA inhibits the migratory ability [...] Read more.
The root bark of Morus alba L. (MA) has been traditionally used for the treatment of various lung diseases in Korea. Although recent research has demonstrated its anticancer effects in several cancer cells, it is still unclear whether MA inhibits the migratory ability of lung cancer cells. The present study investigated the effects of MA on the migration of lung cancer cells and explored the underlying mechanism. Results from a transwell assay and wound-healing assay demonstrated that methylene chloride extracts of MA (MEMA) suppressed the migration and invasion of H1299, H460, and A549 human non-small-cell lung cancer (NSCLC) cells in a concentration-dependent manner. Results from Western blot analyses showed that MEMA reduced the phosphorylation of STAT3 and Src. In addition, MEMA downregulated the expression of epithelial–mesenchymal transition (EMT) marker proteins including Slug, Snail, Vimentin, and N-cadherin, while upregulating the expression of Occludin—a tight-junction protein. The regulation of EMT markers and the decrease of migration by MEMA treatment were reversed once phospho-mimetic STAT3 (Y705D) or Src (Y527F) was transfected into H1299 cells. In conclusions, MEMA inhibited the migratory activity of human NSCLC cells through blocking Src/STAT3-mediated EMT. Full article
(This article belongs to the Special Issue Cancer Cell Reprogramming)
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Review

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17 pages, 1792 KiB  
Review
Understanding the Role of the Transcription Factor Sp1 in Ovarian Cancer: from Theory to Practice
by Balachandar Vellingiri, Mahalaxmi Iyer, Mohana Devi Subramaniam, Kaavya Jayaramayya, Zothan Siama, Bupesh Giridharan, Arul Narayanasamy, Ahmed Abdal Dayem and Ssang-Goo Cho
Int. J. Mol. Sci. 2020, 21(3), 1153; https://doi.org/10.3390/ijms21031153 - 09 Feb 2020
Cited by 60 | Viewed by 5781
Abstract
Ovarian cancer (OC) is one of the deadliest cancers among women contributing to high risk of mortality, mainly owing to delayed detection. There is no specific biomarker for its detection in early stages. However, recent findings show that over-expression of specificity protein 1 [...] Read more.
Ovarian cancer (OC) is one of the deadliest cancers among women contributing to high risk of mortality, mainly owing to delayed detection. There is no specific biomarker for its detection in early stages. However, recent findings show that over-expression of specificity protein 1 (Sp1) is involved in many OC cases. The ubiquitous transcription of Sp1 apparently mediates the maintenance of normal and cancerous biological processes such as cell growth, differentiation, angiogenesis, apoptosis, cellular reprogramming and tumorigenesis. Sp1 exerts its effects on cellular genes containing putative GC–rich Sp1–binding site in their promoters. A better understanding of the mechanisms underlying Sp1 transcription factor (TF) regulation and functions in OC tumorigenesis could help identify novel prognostic markers, to target cancer stem cells (CSCs) by following cellular reprogramming and enable the development of novel therapies for future generations. In this review, we address the structure, function, and biology of Sp1 in normal and cancer cells, underpinning the involvement of Sp1 in OC tumorigenesis. In addition, we have highlighted the influence of Sp1 TF in cellular reprogramming of iPSCs and how it plays a role in controlling CSCs. This review highlights the drugs targeting Sp1 and their action on cancer cells. In conclusion, we predict that research in this direction will be highly beneficial for OC treatment, and chemotherapeutic drugs targeting Sp1 will emerge as a promising therapy for OC. Full article
(This article belongs to the Special Issue Cancer Cell Reprogramming)
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