Hypoxia-enhanced Derivation of iPSCs from Human Dental Pulp Cells

Iida, Kei; Takeda-Kawaguchi, Tomoko; Hada, M.; Yuriguchi, Minoru; Aoki, Hitomi; Tamaoki, Naritaka; Hatakeyama, Daijiro; Kunisada, Takahiro; Shibata, Toshiyuki; Tezuka, Kenichi

doi:10.1177/0022034513502204

Cited by 20 publications

(16 citation statements)

References 27 publications

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“…Although not observed in vivo, E-cadherin is expressed in cultured pulp cells (32). In this study, odontoblastic MDPC-23 cells showed opposite patterns in the expression of Nfic/E-cadherin and TGF-␤/N-cadherin.…”

Section: Discussioncontrasting

confidence: 51%

Nuclear Factor I-C (NFIC) Regulates Dentin Sialophosphoprotein (DSPP) and E-cadherin via Control of Krüppel-like Factor 4 (KLF4) During Dentinogenesis

Lee

Park

et al. 2014

Journal of Biological Chemistry

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Section: Discussioncontrasting

confidence: 51%

Nuclear Factor I-C (NFIC) Regulates Dentin Sialophosphoprotein (DSPP) and E-cadherin via Control of Krüppel-like Factor 4 (KLF4) During Dentinogenesis

Lee

Park

et al. 2014

Journal of Biological Chemistry

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“…RNA extraction (RNeasy Plus Mini Kit; Qiagen) and RT-PCR (Thermal Cycler Dice Real Time System TP800; Takara, Shiga, Japan) were performed as described previously [3] [4] [18] . The mRNA data were normalized to those of GAPDH and used to calculate expression coefficients.…”

Section: Methodsmentioning

confidence: 99%

Derivation of iPSCs after Culture of Human Dental Pulp Cells under Defined Conditions

et al. 2014

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Human dental pulp cells (hDPCs) are a promising resource for regenerative medicine and tissue engineering and can be used for derivation of induced pluripotent stem cells (iPSCs). However, current protocols use reagents of animal origin (mainly fetal bovine serum, FBS) that carry the potential risk of infectious diseases and unwanted immunogenicity. Here, we report a chemically defined protocol to isolate and maintain the growth and differentiation potential of hDPCs. hDPCs cultured under these conditions showed significantly less primary colony formation than those with FBS. Cell culture under stringently defined conditions revealed a donor-dependent growth capacity; however, once established, the differentiation capabilities of the hDPCs were comparable to those observed with FBS. DNA array analyses indicated that the culture conditions robustly altered hDPC gene expression patterns but, more importantly, had little effect on neither pluripotent gene expression nor the efficiency of iPSC induction. The chemically defined culture conditions described herein are not perfect serum replacements, but can be used for the safe establishment of iPSCs and will find utility in applications for cell-based regenerative medicine.

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“…E-cadherin and N-cadherin, both expressed in pulp cells during odontogenesis, are involved in the regulation of various biological processes, such as cell recognition, intercellular communication, cell fate, cell polarity, boundary formation, and morphogenesis [ 36 , 37 ]. In NFI-C −/− mice, KLF4 mRNA expression is significantly decreased compared to wild-type cells.…”

Section: Discussionmentioning

confidence: 99%

Nuclear factor I-C regulates E-cadherin via control of KLF4 in breast cancer

Lee

Park

2015

BMC Cancer

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BackgroundProgression to metastasis is the leading cause of most cancer-related mortality; however, much remains to be understood about what facilitates the spread of tumor cells. In the present study, we describe a novel pathway in breast cancer that regulates epithelial-to-mesenchymal transition (EMT), motility, and invasiveness.MethodsWe examined nuclear factor I-C (NFI-C) expression in MCF10A human breast epithelial cells, MCF7 non-invasive breast cancer cells, and MDA-MB231 invasive breast cancer cells by real-time PCR and western blotting. To investigate the loss- and gain-function of NFI-C, we determined whether NFI-C regulated KLF4 expression by real-time PCR, western blotting, and promoter assay. To understand the biological functions of NFI-C, we observed cell invasion, migration, adhesion in human tumor cells by transwell assay, wound healing assay, quantitative RT-PCR, cell adhesion assay, western blotting, and immunohistochemistry.ResultsWe identified the downstream factors of NFI-C, such as KLF4 and E-cadherin, which play roles in EMT. NFI-C is expressed in normal mammary gland or noninvasive breast cancer cells with epithelial characteristics. NFI-C overexpression induced expression of KLF4 and E-cadherin, but not Slug, in breast cancer cells. NFI-C bound directly to the KLF4 promoter and stimulated KLF4 transcriptional activity, thereby regulating E-cadherin expression during tumorigenesis. Cells overexpressing NFI-C maintained their epithelial differentiation status, which could drive mesenchymal-epithelial transition (MET) via the NFI-C-KLF4-E-cadherin axis in breast cancer cells. Consequently, NFI-C suppressed EMT, migration, and invasion in breast cancer cells.ConclusionsOur study reveals a novel signaling pathway that is important during breast cancer tumorigenesis: the NFI-C-KLF4-E-cadherin pathway. The results indicate the important role of NFI-C in regulating KLF4 during tumorigenesis.

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Hypoxia-enhanced Derivation of iPSCs from Human Dental Pulp Cells

Cited by 20 publications

References 27 publications

Nuclear Factor I-C (NFIC) Regulates Dentin Sialophosphoprotein (DSPP) and E-cadherin via Control of Krüppel-like Factor 4 (KLF4) During Dentinogenesis

Nuclear Factor I-C (NFIC) Regulates Dentin Sialophosphoprotein (DSPP) and E-cadherin via Control of Krüppel-like Factor 4 (KLF4) During Dentinogenesis

Derivation of iPSCs after Culture of Human Dental Pulp Cells under Defined Conditions

Nuclear factor I-C regulates E-cadherin via control of KLF4 in breast cancer

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