Reptin Regulates Pluripotency of Embryonic Stem Cells and Somatic Cell Reprogramming Through Oct4-Dependent Mechanism

Kyoung, Eun; Cheon, Hyo Cheon; Jang, Il Ho; Choi, Eun Jung; Heo, Soon Chul; Kang, Kyung Taek; Bae, Kwang‐Hee; Cho, Yee Sook; Seo, Jeong Kon; Yoon, Jong Hyuk; Lee, Taehoon G.; Kim, Jae Ho

doi:10.1002/stem.1827

Cited by 10 publications

(7 citation statements)

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“…Previous reports have shown that the recruitment of Pontin/Reptin complex increases the transcriptional response of Myc 31 and Oct4 (ref. 32 ), suggesting that this complex modulates transcriptional activity in a number of different cellular and molecular contexts. Mechanistically, Pontin and Reptin are related to a family of AAA + ATPase helicases and they display multiple functions such as the regulation of transcription, DNA repair and chromatin remodelling protein 24 .…”

Section: Discussionmentioning

confidence: 99%

Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression

Tarangelo

Teng

et al. 2015

Nat Commun

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Changes in gene expression during tumorigenesis are often considered the consequence of de novo mutations occurring in the tumour. An alternative possibility is that the transcriptional response of oncogenic transcription factors evolves during tumorigenesis. Here we show that aberrant E2f activity, following inactivation of the Rb gene family in a mouse model of liver cancer, initially activates a robust gene expression programme associated with the cell cycle. Slowly accumulating E2f1 progressively recruits a Pontin/Reptin complex to open the chromatin conformation at E2f target genes and amplifies the E2f transcriptional response. This mechanism enhances the E2f-mediated transactivation of cell cycle genes and initiates the activation of low binding affinity E2f target genes that regulate non-cell-cycle functions, such as the Warburg effect. These data indicate that both the physiological and the oncogenic activities of E2f result in distinct transcriptional responses, which could be exploited to target E2f oncogenic activity for therapy.

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Section: Discussionmentioning

confidence: 99%

Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression

Tarangelo

Teng

et al. 2015

Nat Commun

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“…Using the Lipofectamine-Plus reagent (Life Technologies), pMXs-green fluorescent protein (GFP), pMXs-OCT4, pMXs-SOX2, pMXs-KLF, and pMXs-c-MYC were transfected into prepared PLAT-GP cells (2.5 × 10 4 cells/cm 2 ) with gag-pol and VSV-G [17]. At 4 h after transfection, the medium was replaced with DMEM with 10% FBS.…”

Section: Methodsmentioning

confidence: 99%

Effects of mechanical stimulation on the reprogramming of somatic cells into human-induced pluripotent stem cells

et al. 2017

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BackgroundMechanical stimuli play important roles in the proliferation and differentiation of adult stem cells. However, few studies on their effects on induced pluripotent stem cells (iPSCs) have been published.MethodsHuman dermal fibroblasts were seeded onto flexible membrane-bottom plates, and infected with retrovirus expressing the four reprogramming factors OCT4, SOX2, KLF, and c-MYC (OSKM). The cells were subjected to equiaxial stretching (3% or 8% for 2, 4, or 7 days) and seeded on feeder cells (STO). The reprogramming into iPSCs was evaluated by the expression of pluripotent markers, in vitro differentiation into three germ layers, and teratoma formation.ResultsEquiaxial stretching enhanced reprogramming efficiency without affecting the viral transduction rate. iPSCs induced by transduction of four reprogramming factors and application of equiaxial stretching had characteristics typical of iPSCs in terms of pluripotency and differentiation potentials.ConclusionsThis is the first study to show that mechanical stimuli can increase reprogramming efficiency. However, it did not enhance the infection rate, indicating that mechanical stimuli, defined as stretching in this study, have positive effects on reprogramming rather than on infection. Additional studies should evaluate the mechanism underlying the modulation of reprogramming of somatic cells into iPSCs.

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“…Pontin activation of Oct4 targets is thought to be mediated by recruitment of p300 acetyltransferase (Boo et al, 2015 ). Reptin was also found to maintain pluripotency of ESCs, perhaps acting in complex with Pontin (Do et al, 2014 ) (Table 2 ).…”

Section: Role Of Pontin/reptin In Specific Cellular Pathwaysmentioning

confidence: 99%

The Role of Pontin and Reptin in Cellular Physiology and Cancer Etiology

Mao

Houry

2017

Front. Mol. Biosci.

104

101

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Pontin (RUVBL1, TIP49, TIP49a, Rvb1) and Reptin (RUVBL2, TIP48, TIP49b, Rvb2) are highly conserved ATPases of the AAA+ (ATPases Associated with various cellular Activities) superfamily and are involved in various cellular processes that are important for oncogenesis. First identified as being upregulated in hepatocellular carcinoma and colorectal cancer, their overexpression has since been shown in multiple cancer types such as breast, lung, gastric, esophageal, pancreatic, kidney, bladder as well as lymphatic, and leukemic cancers. However, their exact functions are still quite unknown as they interact with many molecular complexes with vastly different downstream effectors. Within the nucleus, Pontin and Reptin participate in the TIP60 and INO80 complexes important for chromatin remodeling. Although not transcription factors themselves, Pontin and Reptin modulate the transcriptional activities of bona fide proto-oncogenes such as MYC and β-catenin. They associate with proteins involved in DNA damage repair such as PIKK complexes as well as with the core complex of Fanconi anemia pathway. They have also been shown to be important for cell cycle progression, being involved in assembly of telomerase, mitotic spindle, RNA polymerase II, and snoRNPs. When the two ATPases localize to the cytoplasm, they were reported to promote cancer cell invasion and metastasis. Due to their various roles in carcinogenesis, it is not surprising that Pontin and Reptin are proving to be important biomarkers for diagnosis and prognosis of various cancers. They are also current targets for the development of new therapeutic anticancer drugs.

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Reptin Regulates Pluripotency of Embryonic Stem Cells and Somatic Cell Reprogramming Through Oct4-Dependent Mechanism

Cited by 10 publications

References 50 publications

Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression

Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression

Effects of mechanical stimulation on the reprogramming of somatic cells into human-induced pluripotent stem cells

The Role of Pontin and Reptin in Cellular Physiology and Cancer Etiology

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