Cyclins and Cell Cycle Control in Cancer and Disease

Casimiro, Mathew C.; Crosariol, Marco; Loro, Emanuele; Li, Zhiping; Pestell, Richard G.

doi:10.1177/1947601913479022

Cited by 189 publications

(138 citation statements)

References 164 publications

(212 reference statements)

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“…Waf1/Cip1 and cyclin D1, 9 2 cell cycle regulators with effects on tumor invasion, 29,30 we examined whether p21…”

Section: Resultsmentioning

confidence: 99%

KLF4 is downregulated but not mutated during human esophageal squamous cell carcinogenesis and has tumor stage-specific functions

Yang

Katz

2016

Cancer Biology & Therapy

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The transcriptional regulator Kr€ uppel-like factor 4 (KLF4) is decreased in human esophageal squamous cell cancer (ESCC), and Klf4 deletion in mice produces squamous cell dysplasia. Nonetheless the mechanisms of KLF4 downregulation in ESCC and the functions of KLF4 during ESCC development and progression are not well understood. Here, we sought to define the regulation of KLF4 and delineate the stage-specific effects of KLF4 in ESCC. We found that KLF4 expression was decreased in human ESCC and in 8 of 9 human ESCC cell lines. However, by genomic sequencing, we observed no KLF4 mutations or copy number changes in any of 52 human ESCC, suggesting other mechanisms for KLF4 silencing. In fact, KLF4 expression in human ESCC cell lines was increased by the DNA methylation inhibitor 5-azacytidine, suggesting an epigenetic mechanism for KLF4 silencing. Surprisingly, while KLF4 decreased in high-grade dysplasia and early stage tumors, KLF4 increased with advanced cancer stage, and KLF4 expression in ESCC was inversely correlated with survival. Interestingly, KLF4 promoted invasion of human ESCC cells, providing a functional link to the stage-specific expression of KLF4. Taken together, these findings suggest that KLF4 loss is necessary for esophageal tumorigenesis but that restored KLF4 expression in ESCC promotes tumor spread. Thus, the use of KLF4 as a diagnostic and therapeutic target in cancer requires careful consideration of context.Abbreviations: KLF4, Kr€ uppel-like factor 4; ESCC, esophageal squamous cell cancer; SNP, single nucleotide polymorphism; HDAC, histone deacetylase

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“…Waf1/Cip1 and cyclin D1, 9 2 cell cycle regulators with effects on tumor invasion, 29,30 we examined whether p21…”

Section: Resultsmentioning

confidence: 99%

KLF4 is downregulated but not mutated during human esophageal squamous cell carcinogenesis and has tumor stage-specific functions

Yang

Katz

2016

Cancer Biology & Therapy

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“…As loss of quiescence is associated with a failure to maintain long-term self-renewal (45), these data provide a partial explanation for HSC depletion in these animals. B-myb KO LSK + cells express substantially higher levels of CCND1 mRNA, which, in complex with CDK4/6, drives the cell through G 1 and into S-phase (50). It is interesting to note that differentiation of LT-HSCs into ST-HSCs and MPPs, but not HSC self-renewal, correlates with the induction of CCND1 mRNA (18).…”

Section: Discussionmentioning

confidence: 99%

B- myb is an essential regulator of hematopoietic stem cell and myeloid progenitor cell development

Baker

Ma’ayan

Lieu

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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The B-myb (MYBL2) gene is a member of the MYB family of transcription factors and is involved in cell cycle regulation, DNA replication, and maintenance of genomic integrity. However, its function during adult development and hematopoiesis is unknown. We show here that conditional inactivation of B-myb in vivo results in depletion of the hematopoietic stem cell (HSC) pool, leading to profound reductions in mature lymphoid, erythroid, and myeloid cells. This defect is autonomous to the bone marrow and is first evident in stem cells, which accumulate in the S and G 2 /M phases. B-myb inactivation also causes defects in the myeloid progenitor compartment, consisting of depletion of common myeloid progenitors but relative sparing of granulocyte-macrophage progenitors. Microarray studies indicate that B-myb-null LSK + cells differentially express genes that direct myeloid lineage development and commitment, suggesting that B-myb is a key player in controlling cell fate. Collectively, these studies demonstrate that B-myb is essential for HSC and progenitor maintenance and survival during hematopoiesis. myeloipiesis | myelodisplastic syndrome

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“…-downregulated breast cancer cases, cyclin-CDK complex-induced aberrant phosphorylation/inactivation of RB leads to deregulation of E2F1 (77)(78)(79), which is the transcriptional activator for NRBE3. Once the expression of NRBE3 is activated, it in turn targets RB for degradation and forms a positive regulation loop with RB/E2F1.…”

Section: Ink4amentioning

confidence: 99%

A Novel Retinoblastoma Protein (RB) E3 Ubiquitin Ligase (NRBE3) Promotes RB Degradation and Is Transcriptionally Regulated by E2F1 Transcription Factor

Wang

Zheng

Zhang

et al. 2015

Journal of Biological Chemistry

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Background: Retinoblastoma protein (RB) is frequently targeted for proteasomal degradation by oncoproteins. Results: NRBE3 promotes RB degradation as an E3 and is transcriptionally activated by E2F1. Conclusion: NRBE3 is an E3 ubiquitin ligase for RB and regulates the cell cycle. Significance: This study identified a novel E3 ubiquitin ligase for RB that might be a potential oncoprotein in human cancers.

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Cyclins and Cell Cycle Control in Cancer and Disease

Cited by 189 publications

References 164 publications

KLF4 is downregulated but not mutated during human esophageal squamous cell carcinogenesis and has tumor stage-specific functions

KLF4 is downregulated but not mutated during human esophageal squamous cell carcinogenesis and has tumor stage-specific functions

B- myb is an essential regulator of hematopoietic stem cell and myeloid progenitor cell development

A Novel Retinoblastoma Protein (RB) E3 Ubiquitin Ligase (NRBE3) Promotes RB Degradation and Is Transcriptionally Regulated by E2F1 Transcription Factor

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