Somatic Cell Dedifferentiation/Reprogramming for Regenerative Medicine

Ramesh, Thiyagarajan; Lee, Sun Hee; Lee, Choon Soo; Kwon, Yoo Wook; Cho, Hyun Jai

doi:10.15283/ijsc.2009.2.1.18

Cited by 11 publications

(4 citation statements)

References 73 publications

(89 reference statements)

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“…Furthermore, sh-MNX1-AS1 decreased the levels of OCT4, CD33, CD133, and SOX2 in this study, indicating that sh-MNX1-AS1 suppressed the stemness of COAD stem cells. In recent years, somatic cell reprogramming, dedifferentiation, and pluripotent stem cell origin have become the focus of stem cell research [ 33 , 34 ]. Oct4 and Sox2 are the key core regulators for maintaining pluripotency and self-renewal of stem cells [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of LncRNA MNX1-AS1/PPFIA4 Activates AKT/HIF-1α Signal Pathway to Promote Stemness of Colorectal Adenocarcinoma Cells

Sun

Gui

Zhao

et al. 2022

Journal of Oncology

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Purpose. The purpose of this study was to explore the role of the lncRNA MNX1-AS1 and its related downstream signaling pathways in colorectal adenocarcinoma (COAD). Methods. COAD tissues and cells were prepared and treated with sh-MNX1-AS1, pcDNA-MNX1-AS1, sh-PPFIA4, LY29004, and their controls. CCK8 and colony formation assays were undertaken for evaluating cell proliferation. Tumor cell migratory ability was detected by transwell assay. Apoptosis detection was processed by YO-PRO-1/PI Staining. The regulated relationship between lncRNA MNX1-AS1 and PPFIA4 was confirmed by RIP-ChIP assay. Q-PCR was applied to detect genes related to tumor cell stemness, proliferation, migration, and apoptosis in each group. Finally, a xenograft tumor model was constructed to verify the result in vivo. Results. COAD patients with high expression of the lncRNA MNX1-AS1 have poor prognosis. LncRNA MNX1-AS1 promotes the stemness of COAD cells. PPFIA4 mediates lncRNA MNX1-AS1 expression and affects COAD cell stemness. LncRNA MNX1-AS1 accelerates proliferation and migration, while it suppresses apoptosis. LncRNA MNX1-AS1/PPFIA4 accelerates tumor growth in COAD model. LncRNA MNX1-AS1/PPFIA4 activates the downstream AKT/HIF-1α signaling pathway to promote COAD development. LY29004 significantly inhibits the tumorigenic ability of lncRNA MNX1-AS1 and PPFIA4. Conclusion. LncRNA MNX1-AS1/PPFIA4 activates AKT/HIF-1α signal pathway to promote the stemness of COAD cells, which could be a new target for COAD treatment.

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Section: Discussionmentioning

confidence: 99%

Overexpression of LncRNA MNX1-AS1/PPFIA4 Activates AKT/HIF-1α Signal Pathway to Promote Stemness of Colorectal Adenocarcinoma Cells

Sun

Gui

Zhao

et al. 2022

Journal of Oncology

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“…This dedifferentiation technique enables us to obtain donor-or patient-specific pluripotent stem cells (8). In the following section, current methods for dedifferentiation of somatic cells are briefly reviewed.…”

Section: Somatic Cell Dedifferentiationmentioning

confidence: 99%

“…However, mitochondrial DNA from maternal oocytes could be potentially immunogenic (9). Major limitations of this method for clinical application are ethical concerns related to germ cell manipulation, chromosomal disorders in derived stem cells, low efficiency of transfer technique, and insufficient supply of human oocytes (8).…”

Section: Somatic Cell Nuclear Transfer Into Oocytementioning

confidence: 99%

Reprogrammed Cell?based Therapy for Liver Disease: From Lab to Clinic

Mehdizadeh

Darabi

2017

jrenhep

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A large number of patients are affected by liver dysfunction worldwide. Liver transplantation is the only efficient treatment in a variety of enduring liver disorders including inherent and end-stage liver diseases. The generation of human functional hepatocytes in high quantities for liver cell therapy is an important goal for ongoing therapies in regenerative medicine. Reprogrammed cells are considered as a promising and unlimited source of hepatocytes, mainly because of their expected lack of immunogenicity and minimized ethical concerns in clinical applications. Despite gained advances in the reprogramming of somatic cells to functional hepatocytes in vitro, production of primary adult hepatocytes that can proliferate in vivo still remains inaccessible. As part of efforts toward translation of cell reprogramming science into clinical practice, more careful cell selection strategies should be integrated into improvement of dedifferentiation and redifferentiation protocols, especially in precision medicine where gene correction is needed. Furthermore, advances in cellular reprogramming highlight the need for developing and evaluating novel standards addressing clinical research interests in this field.

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“…Many cancerous tumors have long been known to acquire histologic characteristics devoid of the defining features of the tissue of origin. This process of dedifferentiation is characterized by cell regression from a specialized function to a simpler state reminiscent of stem cells [1]. The dedifferentiation of normal cells has long been one theory of the cellular origin of cancers, with the process of dedifferentiation posited to give rise to cancer stem cells; an alternative suggests that cancer stem cells arise from adult stem cells present in the tissues [2].…”

Section: Introductionmentioning

confidence: 99%

Absence of an embryonic stem cell DNA methylation signature in human cancer

et al. 2019

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Background Differentiated cells that arise from stem cells in early development contain DNA methylation features that provide a memory trace of their fetal cell origin (FCO). The FCO signature was developed to estimate the proportion of cells in a mixture of cell types that are of fetal origin and are reminiscent of embryonic stem cell lineage. Here we implemented the FCO signature estimation method to compare the fraction of cells with the FCO signature in tumor tissues and their corresponding nontumor normal tissues. Methods We applied our FCO algorithm to discovery data sets obtained from The Cancer Genome Atlas (TCGA) and replication data sets obtained from the Gene Expression Omnibus (GEO) data repository. Wilcoxon rank sum tests, linear regression models with adjustments for potential confounders and non-parametric randomization-based tests were used to test the association of FCO proportion between tumor tissues and nontumor normal tissues. P -values of < 0.05 were considered statistically significant. Results Across 20 different tumor types we observed a consistently lower FCO signature in tumor tissues compared with nontumor normal tissues, with 18 observed to have significantly lower FCO fractions in tumor tissue (total n = 6,795 tumor, n = 922 nontumor, P < 0.05). We replicated our findings in 15 tumor types using data from independent subjects in 15 publicly available data sets (total n = 740 tumor, n = 424 nontumor, P < 0.05). Conclusions The results suggest that cancer development itself is substantially devoid of recapitulation of normal embryologic processes. Our results emphasize the distinction between DNA methylation in normal tightly regulated stem cell driven differentiation and cancer stem cell reprogramming that involves altered methylation in the service of great cell heterogeneity and plasticity. Electronic supplementary material The online version of this article (10.1186/s12885-019-5932-6) contains supplementary material, which is available to authorized users.

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Somatic Cell Dedifferentiation/Reprogramming for Regenerative Medicine

Cited by 11 publications

References 73 publications

Overexpression of LncRNA MNX1-AS1/PPFIA4 Activates AKT/HIF-1α Signal Pathway to Promote Stemness of Colorectal Adenocarcinoma Cells

Overexpression of LncRNA MNX1-AS1/PPFIA4 Activates AKT/HIF-1α Signal Pathway to Promote Stemness of Colorectal Adenocarcinoma Cells

Reprogrammed Cell?based Therapy for Liver Disease: From Lab to Clinic

Absence of an embryonic stem cell DNA methylation signature in human cancer

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