MAML1 Acts Cooperatively with EGR1 to Activate EGR1-Regulated Promoters: Implications for Nephrogenesis and the Development of Renal Cancer

Hansson, Magnus L.; Behmer, Stefanie; Ceder, Rebecca; Mohammadi, Saeed; Preta, Giulio; Grafström, Roland C.; Fadeel, Bengt; Wallberg, Annika E.

doi:10.1371/journal.pone.0046001

Cited by 20 publications

(22 citation statements)

References 27 publications

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“…In Paper II we suggested a possibility of arsenic been effective against renal cancers overexpressing MAML1 protein. An in silico study has showed that MAML1 expression was increased in renal cancer cell carcinoma and that it correlated with decreased patients' survival (Hansson et al 2012). In this respect, treatment of renal tumor cells overexpressing MAML1 with arsenic could possibly downregulate the levels of MAML1 and decrease cell proliferation, as was reported for HEK293 cells in Paper II.…”

Section: Discussionmentioning

confidence: 61%

“…In the absence of a Wnt signal, the cytoplasmic β-catenin is continuously degraded by the Axis complex (MacDonald, Tamai, and He 2009). Once a Wnt ligand binds to the Frizzled (Fz) receptor, which is a transmembrane protein, and its co-receptor LRP6 protein, the Axis complex is recruited to the reported that MAML1 and KAT2B copy number variances were predominant changes in patients with clear-cell renal cell carcinoma (ccRCC) (Hansson et al 2012;Feng et al 2015).…”

Section: Mastermind-like 1 Protein (Maml1)mentioning

confidence: 99%

“…Disruption of MAML expression or activity has been linked to deregulation of tissues' normal development and tumorigenesis (Watanabe et al 2013;Proweller et al 2006;Kang et al 2013 (Maillard et al 2004;Lizi Wu et al 2007). Moreover, Notch signaling deregulation by MAML proteins has been linked to tumor development, including cutaneous melanoma, neuroblastoma and renal cancer (W. Zhang et al 2015;Heynen et al 2016;Hansson et al 2012). In this respect and considering that ubiquitination can lead to degradation of transcriptional activators' and co-activators'…”

Section: Ubiquitination Of Maml Proteinsmentioning

confidence: 99%

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Arsenic-induced suppression of kidney cell proliferation and the transcriptional coregulator MAML1

Pournara¹,

Holmlund²,

Lu³

et al. 2014

Metallomics

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Mastermind-like 1 (MAML1) is a transcriptional coregulator of diverse/multiple activators, such as Notch, p53, myocyte enhancer factor 2C, NF-κB, beta-catenin, papillomavirus E6 proteins, early growth response 1 and runt-related transcription factor 2. Thus, MAML1 functions in various signaling pathways, most of them connected to cell proliferation, which suggests that MAML1 might play a potential role as a cell proliferation marker. In this study we show that MAML1 expression in the kidney correlates in silico with established cell proliferation markers including PCNA, CDC2 and XRCC5 (Ku80). Over-expression of MAML1 increased proliferation of human embryonic kidney (HEK) 293 cells, while MAML1 downregulation by siRNA decreased cell proliferation. Exposure of HEK293 cells to inorganic arsenic (arsenite) showed reduced levels of MAML1, in combination with a decreased proliferation rate. Our findings provide evidence that arsenic can inhibit proliferation of embryonic kidney cells, possibly through reduction of MAML1 gene expression.

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Section: Discussionmentioning

confidence: 61%

Section: Mastermind-like 1 Protein (Maml1)mentioning

confidence: 99%

Section: Ubiquitination Of Maml Proteinsmentioning

confidence: 99%

See 1 more Smart Citation

Arsenic-induced suppression of kidney cell proliferation and the transcriptional coregulator MAML1

Pournara¹,

Holmlund²,

Lu³

et al. 2014

Metallomics

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“…It could enhance the acetyltransferase activity of p300 and in turn promoted the acetylation of Notch [27]. Also, MAML1 could induce acetylation of the transcription factor early growth response-1 (EGR1) by p300 in embryonic kidney cells [28]. Those results together with that Notch was Network analysis of the Notch gene set in clear cell renal cell carcinoma (ccRCC).…”

Section: Discussionmentioning

confidence: 95%

Genetic alteration in notch pathway is associated with better prognosis in renal cell carcinoma

et al. 2015

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Notch signaling was associated with a variety of cancers but was not comprehensively studied in clear‐cell renal cell carcinoma (ccRCC). We have in this study studied the genetic alteration (mutation and copy number variance) of Notch gene set in the Cancer Genome Atlas (TCGA) Kidney Renal Clear Cell Carcinoma (KIRC) database. We found that Notch pathway was frequently altered in ccRCC. The Notch gene set was genetically altered in 182 (44%) of the 415 ccRCC patients. CNV was the predominant type of alteration in most genes. Alterations in KAT2B and MAML1 occurred in 13% and 19% of patients, respectively, both of which were functionally active in ccRCC. Deletion of VHL was exclusively found in cases with Notch alteration. Overall survival was longer in ccRCC patients with altered‐Notch pathway. The median survival was 90.41 months in Notch‐altered cases and 69.15 in Notch‐unaltered cases (P = 0.0404). The median disease free time was 89.82 months in Notch‐altered cases and 77.27 months in in Notch‐unaltered cases (P = 0.935). Conclusively, Notch signaling was altered in almost half of the ccRCC patients and copy number variances in MAML1 and KAT2B were predominant changes. These findings broadened our understanding of the role of Notch in ccRCC. © 2015 BioFactors, 42(1):41–48, 2016

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“…This exciting finding suggests that EMT and MET are not mutually exclusive, and that WT1 could be an important modulator of the equilibrium between the two states. Interestingly Orai1 expression has been shown to be associated with favorable prognosis in clear cell RCC where genetic and epigenetic alterations in EGR1 expression were associated with survival [126, 127]. However, the extent to which EGR1/WT1-mediated regulation of Ca 2+ signaling components contributes to EMT/MET transitions remains unknown.…”

Section: Dysregulation Of Soce In Cancermentioning

confidence: 99%

EGR-mediated control of STIM expression and function

Gross

Hooper

et al. 2019

Cell Calcium

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Summary Ca2+ is a ubiquitous, dynamic and pluripotent second messenger with highly context-dependent roles in complex cellular processes such as differentiation, proliferation, and cell death [1]. These Ca2+ signals are generated by Ca2+-permeable channels located on the plasma membrane (PM) and endoplasmic reticulum (ER) and shaped by PM- and ER-localized pumps and transporters. Differences in the expression of these Ca2+ homeostasis proteins contribute to cell and context-dependent differences in the spatiotemporal organization of Ca2+ signals and, ultimately, cell fate. This review focuses on the Early Growth Response (EGR) family of zinc finger transcription factors and their role in the transcriptional regulation of Stromal Interaction Molecule (STIM1), a critical regulator of Ca2+ entry in both excitable and non-excitable cells.

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MAML1 Acts Cooperatively with EGR1 to Activate EGR1-Regulated Promoters: Implications for Nephrogenesis and the Development of Renal Cancer

Cited by 20 publications

References 27 publications

Arsenic-induced suppression of kidney cell proliferation and the transcriptional coregulator MAML1

Arsenic-induced suppression of kidney cell proliferation and the transcriptional coregulator MAML1

Genetic alteration in notch pathway is associated with better prognosis in renal cell carcinoma

EGR-mediated control of STIM expression and function

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