Regulation of the protein stability and transcriptional activity of OCT4 in stem cells

Sohn, Eun Jung; Moon, Hye Ji; Lim, Jae Kyong; Kim, Da Sol; Kim, Jae Ho

doi:10.1016/j.jbior.2020.100777

Cited by 11 publications

(3 citation statements)

References 69 publications

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“…Ribosome profiling also offer a quantitative way to investigate translational regulation by post-transcriptional processes that affect protein levels, including protein stability, protein degradation, and others [55] , [56] , [57] , [58] . We applied a deltaTE approach that uses the DESeq2 statistical model to determine the significant changes in interaction term (or ΔTE) under different treatments [24] .…”

Section: Resultsmentioning

confidence: 99%

Integrative analysis of macrophage ribo-Seq and RNA-Seq data define glucocorticoid receptor regulated inflammatory response genes into distinct regulatory classes

Ansari

Dantoft

Ruiz-Orera

et al. 2022

Computational and Structural Biotechnology Journal

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Section: Resultsmentioning

confidence: 99%

Integrative analysis of macrophage ribo-Seq and RNA-Seq data define glucocorticoid receptor regulated inflammatory response genes into distinct regulatory classes

Ansari

Dantoft

Ruiz-Orera

et al. 2022

Computational and Structural Biotechnology Journal

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“…OCT4 expression has been proven to be related to an undifferentiation phenotype of cancers and poor prognosis in tumor patients ( 26 ). OCT4 plays an important role in numerous biological processes such as epigenetic regulation, chromatin remodeling, and transcriptional modulation in embryonic stem cells ( 27 ). For instance, OCT4 collaborated with NCOR1 precipitated transcriptional repression on high expression genes in MEFs ( 22 ).…”

Section: Discussionmentioning

confidence: 99%

HPV16 E6-Activated OCT4 Promotes Cervical Cancer Progression by Suppressing p53 Expression via Co-Repressor NCOR1

Shu

Liu

et al. 2022

Front. Oncol.

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Human papillomaviruses (HPV), mainly HPV16 and HPV18, of high-risk classification are involved in cervical cancer carcinogenesis and progression. Octamer-binding transcription factor 4 (OCT4) is a key transcription factor that is increased in various cancer types. Cervical cancer patients with higher levels of OCT4 had worse survival rates. However, the definite mechanisms underlying its function in the development of cervical cancer still remain to be explicated. Here, our study demonstrated that OCT4 expression was slightly increased in cervical cancer tissues than in precancerous ones. However, OCT4 was significantly upregulated in HPV16-positive tissues, in contrast to the expression profiling for p53. Moreover, knockdown of HPV16 E6 in SiHa cells suppressed the expression of OCT4 with impaired activities of cell proliferation, migration, and invasion, while it recovered the expression of p53. Overexpression of OCT4 and p53 exerted opposite roles on cell proliferation, migration, invasion, and colony formation of cervical cancer cells. More importantly, the enforced expression of OCT4 augmented p53-inhibited cell migration, invasion, and colony formation in human cervical cancer by promoting EMT. Finally, we identified that OCT4 could bind to the p53 promoter region to repress p53 expression by recruiting co-repressor NCOR1 using luciferase, ChIP, and co-IP experiments. We further illustrated that OCT4 not only increased the lung metastasis of cervical cancer but also effectively reversed p53-inhibited lung metastasis. In conclusion, our results suggested that HPV16 E6 activated the expression of OCT4 and subsequently crippled the transcription of p53 via co-repressor NCOR1, which contributed to cervical cancer progression.

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“…Classically, SUMO conjugation consists of the covalent linkage of SUMO protein on lysine residues of a protein substrate, which is triggered by the sequential action of three enzymes: heterodimeric E1-activating enzyme (Aos1/Uba2), E2-conjugating enzyme (Ubc9), and SUMO-E3 ligase, in an ATP-dependent manner ( Streich and Lima, 2014 ; Pichler et al, 2017 ; Varejão et al, 2020 ). SUMO-conjugated maintains the fine-tuning of cellular functions by altering intracellular compartmentalization or modulating the protein stability, enzymatic activity, and interactions affinity ( Moreno-Oñate et al, 2020 ; Sohn et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Targeting SUMOylation in Plasmodium as a Potential Target for Malaria Therapy

Oliveira

Kronenberger

Palmisano

et al. 2021

Front. Cell. Infect. Microbiol.

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Malaria is a parasitic disease that represents a public health problem worldwide. Protozoans of the Plasmodium genus are responsible for causing malaria in humans. Plasmodium species have a complex life cycle that requires post-translational modifications (PTMs) to control cellular activities temporally and spatially and regulate the levels of critical proteins and cellular mechanisms for maintaining an efficient infection and immune evasion. SUMOylation is a PTM formed by the covalent linkage of a small ubiquitin-like modifier protein to the lysine residues on the protein substrate. This PTM is reversible and is triggered by the sequential action of three enzymes: E1-activating, E2-conjugating, and E3 ligase. On the other end, ubiquitin-like-protein-specific proteases in yeast and sentrin-specific proteases in mammals are responsible for processing SUMO peptides and for deconjugating SUMOylated moieties. Further studies are necessary to comprehend the molecular mechanisms and cellular functions of SUMO in Plasmodium. The emergence of drug-resistant malaria parasites prompts the discovery of new targets and antimalarial drugs with novel mechanisms of action. In this scenario, the conserved biological processes regulated by SUMOylation in the malaria parasites such as gene expression regulation, oxidative stress response, ubiquitylation, and proteasome pathways, suggest PfSUMO as a new potential drug target. This mini-review focuses on the current understanding of the mechanism of action of the PfSUMO during the coordinated multi-step life cycle of Plasmodium and discusses them as attractive new target proteins for the development of parasite-specific inhibitors and therapeutic intervention toward malaria disease.

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Regulation of the protein stability and transcriptional activity of OCT4 in stem cells

Cited by 11 publications

References 69 publications

Integrative analysis of macrophage ribo-Seq and RNA-Seq data define glucocorticoid receptor regulated inflammatory response genes into distinct regulatory classes

Integrative analysis of macrophage ribo-Seq and RNA-Seq data define glucocorticoid receptor regulated inflammatory response genes into distinct regulatory classes

HPV16 E6-Activated OCT4 Promotes Cervical Cancer Progression by Suppressing p53 Expression via Co-Repressor NCOR1

Targeting SUMOylation in Plasmodium as a Potential Target for Malaria Therapy

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