Ctr9, a key subunit of PAFc, affects global estrogen signaling and drives ERα-positive breast tumorigenesis

Zeng, Hao; Xu, Wei

doi:10.1101/gad.268722.115

Cited by 32 publications

(57 citation statements)

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“…For instance, the human PAFc is required for the maintenance of embryonic stem cell identity [11], neuronal migration in mammalian brain [12], antiviral and pro-inflammatory response [13], and oncogenesis regulation [14, 15]. Our studies have demonstrated the involvement of Ctr9, a key scaffold subunit of human PAFc, in ERα-positive breast cancer progression and ERα target gene expression [16]. Specifically, using loss-of-function approach, we observed that depletion of Ctr9 led to apparent morphological change, decrease of proliferation, reduced colony formation, and impaired ERα-target gene expression in ERα-positive breast cancer cells [16].…”

Section: Introductionmentioning

confidence: 99%

“…Our studies have demonstrated the involvement of Ctr9, a key scaffold subunit of human PAFc, in ERα-positive breast cancer progression and ERα target gene expression [16]. Specifically, using loss-of-function approach, we observed that depletion of Ctr9 led to apparent morphological change, decrease of proliferation, reduced colony formation, and impaired ERα-target gene expression in ERα-positive breast cancer cells [16]. Moreover, Ctr9 regulates ERα protein stability and facilitates RNAPII recruitment and transcription-coupled histone modifications such as H2Bub1, H3K27ac, and H3K36me3 at the selected ERα targets [16].…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, using loss-of-function approach, we observed that depletion of Ctr9 led to apparent morphological change, decrease of proliferation, reduced colony formation, and impaired ERα-target gene expression in ERα-positive breast cancer cells [16]. Moreover, Ctr9 regulates ERα protein stability and facilitates RNAPII recruitment and transcription-coupled histone modifications such as H2Bub1, H3K27ac, and H3K36me3 at the selected ERα targets [16]. However, the global control of Ctr9 on ERα occupancy and RNAPII recruitment awaits investigation to deeply understand the functional significance of Ctr9 in ERα transcription network in breast cancer.…”

Section: Introductionmentioning

confidence: 99%

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Systematic identification of Ctr9 regulome in ERα-positive breast cancer

et al. 2016

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BackgroundWe had previously identified Ctr9, the key scaffold subunit of the human RNA polymerase II (RNAPII) associated factor complex (PAFc), as a key factor regulating a massive ERα target gene expression and ERα-positive breast cancer growth. Furthermore, we have shown that knockdown of Ctr9 reduces ERα protein stability and decreases the occupancy of ERα and RNAPII at a few ERα-target loci. However, it remains to be determined whether Ctr9 controls ERα-target gene expression by regulating the global chromatin occupancy of ERα and RNAPII in the presence of estrogen.ResultsIn this study, we determined the genome-wide ERα and RNAPII occupancy in response to estrogen treatment and/or Ctr9 knockdown by performing chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq). We found that loss of Ctr9 dramatically decreases the global occupancy of ERα and RNAPII, highlighting the significance of Ctr9 in regulating estrogen signaling in ERα-positive breast cancer cells. Combining this resource with previously published genomic data sets, we identified a unique subset of ERα and Ctr9 target genes, and further delineated the independent function of Ctr9 from other subunits in PAFc when regulating transcription.ConclusionsOur data demonstrated that Ctr9, independent of other PAFc subunits, controls ERα-target gene expression by regulating global chromatin occupancies of ERα and RNAPII.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-3248-3) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Systematic identification of Ctr9 regulome in ERα-positive breast cancer

et al. 2016

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“…Inanition, several studies have suggested relations between Wnt or Notch signaling and different components of Paf1C [233][234][235][236]. Further, some of the Paf1C components e.g., Ctr9 are identified as a tumor suppressor factor in various organisms especially in human [232,[237][238][239][240][241].…”

Section: Mapping By Wgsmentioning

confidence: 99%

“…Additionally, studies in mammals showed that Ctr9 is necessary for early human development (implantation), and loss-of-function of hCtr9 results in the reduction of H3K36 trimethylation [223]. In addition, Ctr9 is identified as a tumor suppressor factor e.g., studies on human identified mutations in Ctr9 to be liable for Wilms tumor i.e., embryonal kidney cancer [238], and some types of breast cancer [241].…”

Section: Ctr9 a Key Components Of Paf1cmentioning

confidence: 99%

Genetic mechanisms regulating proliferation and cell specification in the Drosophila embryonic CNS

Bahrampour¹

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Cover picture/illustration: Confocal image of the Drosophila embryos fillets at stage 12, stained for Dpn (green), Pros (red), GsbN (blue) and PH3 (white). The front cover shows the control, and the back cover is the combinatorial misexpression of da-Gal/UAS-ase, -SoxN, -wor, -hb, -Kr, -nub leads to the widespread generation of NBs and GMCs, and extensive proliferation throughout the ectoderm, contrary the underlying VNC shows normal segmentation.Published articles have been reprinted with the permission of the copyright holder.Printed in Sweden by LiU-Tryck, Linköping, Sweden, 2017

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CTR9‐mediated JAK2/STAT3 pathway promotes the proliferation, migration, and invasion of human glioma cells

Chen

et al. 2021

Clinical Laboratory Analysis

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Background CTR9 (Cln three requiring 9) has been reported to be implicated in protein modification and oncogenesis of several human cancers. However, the protein expression and mechanism of CTR9 in glioma progression remain unclear. Methods We analyzed mRNA expression of CTR9 and CTR9‐related survival curves in the public database. Then, we detected CTR9 expression in glioma tissues and constructed U251 and U87 cells with stable silencing or overexpression of CTR9. Cell function tests and Western blot were conducted to explore the effects of CTR9 on glioma proliferation, invasion and migration, and the specific mechanism. All the date was presented as means ± SEM. Two‐sample t test and one‐way analysis of variance (ANOVA) were used to identify whether there was a significant difference between each group of data. Results We found that CTR9 was overexpressed in glioma and inversely associated with glioma patient survival. The results manifested that knockdown of CTR9 suppressed the proliferation, migration, and invasion of glioma cells, while overexpression facilitated them. The underlying molecular mechanism may involve the regulation of JAK2/STAT3 pathway by CTR9. Conclusion Our present study indicates that CTR9 is highly expressed in glioma and related to glioma grading and prognosis. CTR9 regulates malignant behaviors of glioma cells by activating JAK2/STAT3 pathway. Therefore, CTR9 may be a promising biomarker for the targeted therapy and prognosis evaluation of glioma.

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Ctr9, a key subunit of PAFc, affects global estrogen signaling and drives ERα-positive breast tumorigenesis

Cited by 32 publications

References 51 publications

Systematic identification of Ctr9 regulome in ERα-positive breast cancer

Systematic identification of Ctr9 regulome in ERα-positive breast cancer

Genetic mechanisms regulating proliferation and cell specification in the Drosophila embryonic CNS

CTR9‐mediated JAK2/STAT3 pathway promotes the proliferation, migration, and invasion of human glioma cells

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