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Journal articles on the topic 'ETV4'

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Author: Grafiati

Published: 10 March 2023

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1

Eo, Jinwon, Kyuyong Han, Kenneth M Murphy, Haengseok Song, and Hyunjung Jade Lim. "Etv5, an ETS transcription factor, is expressed in granulosa and cumulus cells and serves as a transcriptional regulator of the cyclooxygenase-2." Journal of Endocrinology 198, no. 2 (May 20, 2008): 281–90. http://dx.doi.org/10.1677/joe-08-0142.

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Etv4, Etv1, and Etv5 are members of Etv4 subfamily of E26 transformation-specific (Ets) transcription factors that are known to influence a host of biological processes. We previously showed that Etv5, expressed in Sertoli cells, plays a crucial role in maintaining spermatogonial stem cell niche in the mouse testis. However, it is not yet known whether Etv4 family members are expressed in the ovary or play any role in ovarian functions. Here, we show that Etv5 and Etv4 are expressed in mouse ovaries in granulosa and cumulus cells during folliculogenesis. Both Etv5 and Etv4 mRNAs are also detected in cumulus–oocyte complexes (COCs) and denuded oocytes. Notably, Etv4 is highly expressed in the cumulus cells of ovulated COCs at 16-h post-human chorionic gonadotropin. Cyclooxygenase-2 (PTGS2), a rate-limiting enzyme for prostaglandin synthesis, is critical for oocyte maturation and ovulation. Since several putative Ets-binding sites are present in the PTGS2 promoter, we examined whether Etv5 influences Ptgs2 transcriptional activity. Indeed, we found that addition of Etv5 increases the transcriptional activity of the 3.2-kb mouse Ptgs2 promoter by 2.5-fold in luciferase reporter assays. Collectively, the results show that Etv4 and Etv5 are expressed in granulosa and cumulus cells during folliculogenesis and ovulation, suggesting that they influence cellular events in the ovary by regulating downstream genes such as Ptgs2.

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2

Newton, Kim, Debra L. Dugger, Arundhati Sengupta-Ghosh, Ronald E. Ferrando, Felix Chu, Janet Tao, Wendy Lam, et al. "Ubiquitin ligase COP1 coordinates transcriptional programs that control cell type specification in the developing mouse brain." Proceedings of the National Academy of Sciences 115, no. 44 (October 15, 2018): 11244–49. http://dx.doi.org/10.1073/pnas.1805033115.

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The E3 ubiquitin ligase CRL4COP1/DET1 is active in the absence of ERK signaling, modifying the transcription factors ETV1, ETV4, ETV5, and c-JUN with polyubiquitin that targets them for proteasomal degradation. Here we show that this posttranslational regulatory mechanism is active in neurons, with ETV5 and c-JUN accumulating within minutes of ERK activation. Mice with constitutive photomorphogenesis 1 (Cop1) deleted in neural stem cells showed abnormally elevated expression of ETV1, ETV4, ETV5, and c-JUN in the developing brain and spinal cord. Expression of c-JUN target genes Vimentin and Gfap was increased, whereas ETV5 and c-JUN both contributed to an expanded number of cells expressing genes associated with gliogenesis, including Olig1, Olig2, and Sox10. The mice had subtle morphological abnormalities in the cerebral cortex, hippocampus, and cerebellum by embryonic day 18 and died soon after birth. Elevated c-JUN, ETV5, and ETV1 contributed to the perinatal lethality, as several Cop1-deficient mice also lacking c-Jun and Etv5, or lacking Etv5 and heterozygous for Etv1, were viable.

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3

Dissanayake, Kumara, Rachel Toth, Jamie Blakey, Olof Olsson, David G. Campbell, Alan R. Prescott, and Carol MacKintosh. "ERK/p90RSK/14-3-3 signalling has an impact on expression of PEA3 Ets transcription factors via the transcriptional repressor capicúa." Biochemical Journal 433, no. 3 (January 14, 2011): 515–25. http://dx.doi.org/10.1042/bj20101562.

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Compounds that inhibit signalling upstream of ERK (extracellular-signal-regulated kinase) are promising anticancer therapies, motivating research to define how this pathway promotes cancers. In the present study, we show that human capicúa represses mRNA expression for PEA3 (polyoma enhancer activator 3) Ets transcription factors ETV1, ETV4 and ETV5 (ETV is Ets translocation variant), and this repression is relieved by multisite controls of capicúa by ERK, p90RSK (p90 ribosomal S6 kinase) and 14-3-3 proteins. Specifically, 14-3-3 binds to p90RSK-phosphorylated Ser173 of capicúa thereby modulating DNA binding to its HMG (high-mobility group) box, whereas ERK phosphorylations prevent binding of a C-terminal NLS (nuclear localization sequence) to importin α4 (KPNA3). ETV1, ETV4 and ETV5 mRNA levels in melanoma cells are elevated by siRNA (small interfering RNA) knockdown of capicúa, and decreased by inhibiting ERK and/or expressing a form of capicúa that cannot bind to 14-3-3 proteins. Capicúa knockdown also enhances cell migration. The findings of the present study give further mechanistic insights into why ETV1 is highly expressed in certain cancers, indicate that loss of capicúa can desensitize cells to the effects of ERK pathway inhibitors, and highlight interconnections among growth factor signalling, spinocerebellar ataxias and cancers.

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4

Schmerr, Martin, Sune Kobberup, Ngai Woo, and Jan Jensen. "Role of Etv4 and Etv5 in pancreatic development." Developmental Biology 356, no. 1 (August 2011): 168. http://dx.doi.org/10.1016/j.ydbio.2011.05.622.

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5

Babal, Yigit Koray, Basak Kandemir, and Isil Aksan Kurnaz. "Gene Regulatory Network of ETS Domain Transcription Factors in Different Stages of Glioma." Journal of Personalized Medicine 11, no. 2 (February 17, 2021): 138. http://dx.doi.org/10.3390/jpm11020138.

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The ETS domain family of transcription factors is involved in a number of biological processes, and is commonly misregulated in various forms of cancer. Using microarray datasets from patients with different grades of glioma, we have analyzed the expression profiles of various ETS genes, and have identified ETV1, ELK3, ETV4, ELF4, and ETV6 as novel biomarkers for the identification of different glioma grades. We have further analyzed the gene regulatory networks of ETS transcription factors and compared them to previous microarray studies, where Elk-1-VP16 or PEA3-VP16 were overexpressed in neuroblastoma cell lines, and we identify unique and common regulatory networks for these ETS proteins.

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6

Currie, Simon L., Desmond K. W. Lau, Jedediah J. Doane, Frank G. Whitby, Mark Okon, Lawrence P. McIntosh, and Barbara J. Graves. "Structured and disordered regions cooperatively mediate DNA-binding autoinhibition of ETS factors ETV1, ETV4 and ETV5." Nucleic Acids Research 45, no. 5 (February 6, 2017): 2223–41. http://dx.doi.org/10.1093/nar/gkx068.

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7

Cooper, Christopher D. O., Joseph A. Newman, Hazel Aitkenhead, Charles K. Allerston, and Opher Gileadi. "Structures of the Ets Protein DNA-binding Domains of Transcription Factors Etv1, Etv4, Etv5, and Fev." Journal of Biological Chemistry 290, no. 22 (April 12, 2015): 13692–709. http://dx.doi.org/10.1074/jbc.m115.646737.

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8

Shin, Ye Ji, Jae Won Yun, and Hong Sook Kim. "Portrait of Molecular Signaling and Putative Therapeutic Targets in Prostate Cancer with ETV4 Fusion." Biomedicines 10, no. 10 (October 20, 2022): 2650. http://dx.doi.org/10.3390/biomedicines10102650.

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Gene fusion between androgen receptor (AR) response genes and E26 transformation-specific (ETS) family members increases the gene expression of ETS family members, and promotes tumorigenesis in prostate cancer. However, the molecular features of ETV4 fusion in prostate cancer are not fully understood, and drugs targeting ETV4 fusion have not been developed. To examine key cellular signaling pathways and explore therapeutic targets and drugs for ETV4-fusion-positive prostate cancer, we analyzed RNA sequencing data and clinical information for prostate cancer. The ETV4-fusion-positive group was selected through prior study and analysis comparing ETV4-fusion-positive and -negative groups was conducted using a Pearson correlation test. We obtained 393 genes correlated with ETV4 expression. Pathway analysis was performed using over-representation analysis (ORA), and six cancer-specific molecular signaling pathways (the irinotecan pathway, metabolism, androgen receptor signaling, interferon signaling, MAPK/NF-kB signaling, and the tamoxifen pathway) were altered in the ETV4-fusion-positive group. Furthermore, a gene–drug database was used to find an actionable drug and therapeutic target for the ETV4-fusion-positive group. Here, we have identified significantly altered genes and oncogenic signaling pathways in ETV4-fusion-positive prostate cancer, and we suggest therapeutic targets and potential drugs for ETV4-fusion-positive prostate patients.

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9

Zhang, Xueming, Lei Si, Zhanpeng Yue, Yang Liu, Bin Guo, Ziyi Li, and Dexue Li. "Expression of Ets Transcription Factors Etv4, Etv1 in Mouse Testis." Biology of Reproduction 83, Suppl_1 (November 1, 2010): 517. http://dx.doi.org/10.1093/biolreprod/83.s1.517.

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10

Chen, Jing, Amelie T. Van der Ven, Joseph A. Newman, Asaf Vivante, Nina Mann, Hazel Aitkenhead, Shirlee Shril, et al. "ETV4 Mutation in a Patient with Congenital Anomalies of the Kidney and Urinary Tract." International Journal of Pediatrics and Child Health 4, no. 2 (September 4, 2016): 61–71. http://dx.doi.org/10.12974/2311-8687.2016.04.02.1.

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Congenital anomalies of the kidney and urinary tract (CAKUT) are the most common reason for chronic kidney disease in children. Although more than 30 monogenic causes have been implicated in isolated forms of human CAKUT so far, the vast majority remains elusive. To identify novel monogenic causes of CAKUT we applied homozygosity mapping, together with whole exome sequencing, in a patient from consanguineous descent with isolated CAKUT. We identified a homozygous missense mutation (p.Arg415His) of the Ets Translocation Variant Gene 4 (ETV4). The transcription factor ETV4 is a downstream target of the GDNF/RET signaling pathway that plays a crucial role in kidney development. We show by means of electrophoretic mobility shift assay that the Arg415His mutant causes loss of the DNA binding affinity of ETV4 and fails to activate transcription in a cell-based luciferase reporter assay. We furthermore investigated the impact of the mutant protein on cell migration rate. Unlike wildtype ETV4, the Arg415His mutant failed to rescue cell migration defects observed in two ETV4 knock-down cell-lines. We therefore identified and functionally characterized a recessive mutation in ETV4 in a human patient with CAKUT. We hypothesize that the pathomechanism of this mutation could be via loss of the transcriptional function of ETV4, and a resulting abrogation of GDNF/RET/ETV4 signaling pathway.

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11

Barros-Silva, Joao D., Paula Paulo, Anne Cathrine Bakken, Nuno Cerveira, Marthe Løvf, Rui Henrique, Carmen Jerönimo, Ragnhild A. Lothe, Rolf Inge Skotheim, and Manuel R. Teixeira. "Novel 5′ Fusion Partners of ETV1 and ETV4 in Prostate Cancer." Neoplasia 15, no. 7 (July 2013): 720—IN6. http://dx.doi.org/10.1593/neo.13232.

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12

Kunju, Lakshmi P., Shannon Carskadon, Javed Siddiqui, Scott A. Tomlins, Arul M. Chinnaiyan, and Nallasivam Palanisamy. "Novel RNA Hybridization Method for the In Situ Detection of ETV1, ETV4, and ETV5 Gene Fusions in Prostate Cancer." Applied Immunohistochemistry & Molecular Morphology 22, no. 8 (September 2014): e32-e40. http://dx.doi.org/10.1097/pai.0000000000000095.

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13

Aguilar-Martinez, Elisa, Baoqiang Guo, and Andrew D. Sharrocks. "RNF4 interacts with multiSUMOylated ETV4." Wellcome Open Research 1 (November 15, 2016): 3. http://dx.doi.org/10.12688/wellcomeopenres.9935.1.

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Protein SUMOylation represents an important regulatory event that changes the activities of numerous proteins. Recent evidence demonstrates that polySUMO chains can act as a trigger to direct the ubiquitin ligase RNF4 to substrates to cause their turnover through the ubiquitin pathway. RNF4 uses multiple SUMO interaction motifs (SIMs) to bind to these chains. However, in addition to polySUMO chains, a multimeric binding surface created by the simultaneous SUMOylation of multiple residues on a protein or complex could also provide a platform for the recruitment of multi-SIM proteins like RNF4. Here we demonstrate that multiSUMOylated ETV4 can bind to RNF4 and that a unique combination of SIMs is required for RNF4 to interact with this multiSUMOylated platform. Thus RNF4 can bind to proteins that are either polySUMOylated through a single site or multiSUMOylated on several sites and raises the possibility that such multiSIM-multiSUMO interactions might be more widespread.

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14

Aguilar-Martinez, Elisa, Baoqiang Guo, and Andrew D. Sharrocks. "RNF4 interacts with multiSUMOylated ETV4." Wellcome Open Research 1 (February 17, 2017): 3. http://dx.doi.org/10.12688/wellcomeopenres.9935.2.

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Protein SUMOylation represents an important regulatory event that changes the activities of numerous proteins. Recent evidence demonstrates that polySUMO chains can act as a trigger to direct the ubiquitin ligase RNF4 to substrates to cause their turnover through the ubiquitin pathway. RNF4 uses multiple SUMO interaction motifs (SIMs) to bind to these chains. However, in addition to polySUMO chains, a multimeric binding surface created by the simultaneous SUMOylation of multiple residues on a protein or complex could also provide a platform for the recruitment of multi-SIM proteins like RNF4. Here we demonstrate that multiSUMOylated ETV4 can bind to RNF4 and that a unique combination of SIMs is required for RNF4 to interact with this multiSUMOylated platform. Thus RNF4 can bind to proteins that are either polySUMOylated through a single site or multiSUMOylated on several sites and raises the possibility that such multiSIM-multiSUMO interactions might be more widespread.

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15

Lu, Benson C., Cristina Cebrian, Xuan Chi, Satu Kuure, Richard Kuo, Carlton M. Bates, Silvia Arber, et al. "Etv4 and Etv5 are required downstream of GDNF and Ret for kidney branching morphogenesis." Nature Genetics 41, no. 12 (November 8, 2009): 1295–302. http://dx.doi.org/10.1038/ng.476.

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16

Xiao, Jie, Shu Yang, Ping Shen, Yaxi Wang, Haimei Sun, Fengqing Ji, and Deshan Zhou. "Phosphorylation of ETV4 at Ser73 by ERK kinase could block ETV4 ubiquitination degradation in colorectal cancer." Biochemical and Biophysical Research Communications 486, no. 4 (May 2017): 1062–68. http://dx.doi.org/10.1016/j.bbrc.2017.03.163.

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17

Zhang, Yan, Shigetoshi Yokoyama, John C. Herriges, Zhen Zhang, Randee E. Young, Jamie M. Verheyden, and Xin Sun. "E3 ubiquitin ligase RFWD2 controls lung branching through protein-level regulation of ETV transcription factors." Proceedings of the National Academy of Sciences 113, no. 27 (June 22, 2016): 7557–62. http://dx.doi.org/10.1073/pnas.1603310113.

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The mammalian lung is an elaborate branching organ, and it forms following a highly stereotypical morphogenesis program. It is well established that precise control at the transcript level is a key genetic underpinning of lung branching. In comparison, little is known about how regulation at the protein level may play a role. Ring finger and WD domain 2 (RFWD2, also termed COP1) is an E3 ubiquitin ligase that modifies specific target proteins, priming their degradation via the ubiquitin proteasome system. RFWD2 is known to function in the adult in pathogenic processes such as tumorigenesis. Here, we show that prenatal inactivation of Rfwd2 gene in the lung epithelium led to a striking halt in branching morphogenesis shortly after secondary branch formation. This defect is accompanied by distalization of the lung epithelium while growth and cellular differentiation still occurred. In the mutant lung, two E26 transformation-specific (ETS) transcription factors essential for normal lung branching, ETS translocation variant 4 (ETV4) and ETV5, were up-regulated at the protein level, but not at the transcript level. Introduction of Etv loss-of-function alleles into the Rfwd2 mutant background attenuated the branching phenotype, suggesting that RFWD2 functions, at least in part, through degrading ETV proteins. Because a number of E3 ligases are known to target factors important for lung development, our findings provide a preview of protein-level regulatory network essential for lung branching morphogenesis.

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18

Fontanet, Paula Aldana, Antonella Soledad Ríos, Fernando Cruz Alsina, Gustavo Paratcha, and Fernanda Ledda. "Pea3 Transcription Factors, Etv4 and Etv5, Are Required for Proper Hippocampal Dendrite Development and Plasticity." Cerebral Cortex 28, no. 1 (December 1, 2016): 236–49. http://dx.doi.org/10.1093/cercor/bhw372.

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19

Lu, Benson C., Cristina Cebrian, Xuan Chi, Satu Kuure, Richard Kuo, Carlton M. Bates, Silvia Arber, et al. "Erratum: Etv4 and Etv5 are required downstream of GDNF and Ret for kidney branching morphogenesis." Nature Genetics 42, no. 4 (April 2010): 361. http://dx.doi.org/10.1038/ng0410-361d.

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20

LeBlanc, V. G., S. Chittaranjan, M. Firme, S. Y. Chan, J. Song, A. Lee, S. Yip, and M. A. Marra. "PS2 - 167 CIC Deficiency is Associated with Dysregulation of Genes Involved in Cell Adhesion and Developmental Processes." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 43, S4 (October 2016): S13. http://dx.doi.org/10.1017/cjn.2016.365.

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Somatic mutations in the Capicua (CIC) gene were first identified in Type I low-grade gliomas (LGGs), which are characterized by 1p/19q co-deletions and IDH mutations. They are found at frequencies of ~50-70% in this glioma subtype, and have since been identified in ~40% of stomach adenocarcinomas (STADs) of the microsatellite instability (MSI) subtype; however, the role of these somatic mutations in malignancy has yet to be established. In Drosophila, CIC functions as a transcriptional repressor whose activity is inhibited upon activation of the mitogen-activated protein kinase (MAPK) signalling pathway. Though mammalian CIC appears to retain these functions, only three of its target genes have been established in human cells: ETV1, ETV4, and ETV5 (ETV1/4/5). To further probe CIC’s transcriptional network, we developed CIC knockout cell lines and performed transcriptomic and proteiomic analyses in these and in control cell lines expressing wild type CIC, identifying a total of 582 differentially expressed genes. We also used RNA-seq data from The Cancer Genome Atlas (TCGA) for Type I LGGs and STADs to perform additional differential expression analyses between CIC-deficient and CIC-expressing samples. Though gene-level overlap was limited between the three contexts, we found that CIC appears to regulate the expression of genes involved in cell-cell adhesion, metabolism, and developmental processes in all three contexts. These results shed light on the pathological role of CIC mutations and may help explain why these have been associated with poorer outcome within Type I LGGs.

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21

Deshmukh, Sachin Kumar, Ajay P. Singh, and Seema Singh. "ETV4: an emerging target in pancreatic cancer." Oncoscience 5, no. 9-10 (October 11, 2018): 260–61. http://dx.doi.org/10.18632/oncoscience.471.

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22

Omar, Mohamed, Zhuoran Xu, Ryan Carelli, Jacob Rosenthal, David Brundage, Daniela C. Salles, Eddie L. Imada, et al. "Abstract 462: Using attention-based deep multiple instance learning to identify key genetic alterations in prostate cancer from whole slide images." Cancer Research 82, no. 12_Supplement (June 15, 2022): 462. http://dx.doi.org/10.1158/1538-7445.am2022-462.

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Abstract Prostate cancer (PCa) is associated with several genetic alterations which play an important role in the disease heterogeneity and clinical outcome. These alterations involve gene fusion between TMPRSS2 and members of the ETS family of transcription factors like ERG, ETV1, and ETV4 together with mutations or deletions in tumor suppressors like TP53 and PTEN. The expanding wealth of digital whole slide images (WSIs) and the increasing adoption of deep learning approaches offer a unique opportunity for pathologists to streamline the detection of these alterations. Here, we used 736 haematoxylin and eosin-stained WSIs from 494 primary PCa patients to identify several key genetic alterations including ERG, ETV1, and ETV4 fusion, PTEN loss, and TP53 and SPOP mutations. Using a custom segmentation pipeline, we identified tissue regions and tiled them into high-resolution (10X magnification) patches (256X256 pixels) which were passed to our deep multiple instance learning framework. Using a pre-trained ResNet50 model, we extracted informative features which were subsequently used for training to predict slide-level labels and to detect slide regions with high diagnostic relevance. Using a 10-folds cross validation approach, we divided the data into training (80%), validation (10%) and testing (10%) sets. The training and validation data were used for training the model and hyperparameters tuning, respectively while the testing data was used to provide an unbiased evaluation of the models’ performance using the mean Area Under the Receiver Operating Characteristic (AUROC) across the ten testing folds as evaluation metric. We managed to accurately detect key molecular alterations including ERG fusion, ETV1 fusion, ETV4 fusion, and PTEN loss. Additionally, we were able to detect mutations in TP53 and SPOP together with the presence of androgen-receptor splice variant 7 (ARv7). In addition to slide-level classification, we also identified subregions with high attention score which can help pathologists identify the distinct morphological features associated with each genetic alteration. Finally, in order to examine the cellular structure associated with each genetic alteration, we used Hover-Net model to segment and classify the nuclei in the high-attention tiles. Our work highlights the utility of using WSIs to accurately identify key molecular alteration in cancer and their associated morphological and cellular features on the slide which would streamline the diagnostic process. To the best of our knowledge, this is the first study that uses routine WSIs to predict and characterize key genetic alterations in PCa. Citation Format: Mohamed Omar, Zhuoran Xu, Ryan Carelli, Jacob Rosenthal, David Brundage, Daniela C. Salles, Eddie L. Imada, Renato Umeton, Edward M. Schaeffer, Brian D. Robinson, Tamara L. Lotan, Massimo Loda, Luigi Marchionni. Using attention-based deep multiple instance learning to identify key genetic alterations in prostate cancer from whole slide images [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 462.

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23

Sims-Lucas, Sunder, Luise Cullen-McEwen, Veraragavan P. Eswarakumar, David Hains, Kayle Kish, Brian Becknell, Jue Zhang, John F. Bertram, Fen Wang, and Carlton M. Bates. "Deletion of Frs2α from the ureteric epithelium causes renal hypoplasia." American Journal of Physiology-Renal Physiology 297, no. 5 (November 2009): F1208—F1219. http://dx.doi.org/10.1152/ajprenal.00262.2009.

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Fibroblast growth factor receptor 2 (Fgfr2) signaling is critical in maintaining ureteric branching architecture and mesenchymal stromal morphogenesis in the kidney. Fibroblast growth factor receptor substrate 2α (Frs2α) is a major docking protein for Fgfr2 with downstream targets including Ets variant (Etv) 4 and Etv5 in other systems. Furthermore, global deletion of Frs2α causes early embryonic lethality. The purpose of the study was to determine the role of Frs2α in mediating Fgfr2 signaling in the ureteric epithelium. To that end, we generated mice with conditional deletion of Frs2α in the ureteric epithelium ( Frs2α UB−/−) and mice with point mutations in the Frs2α binding site of Fgfr2 ( Fgfr2 LR/LR). Frs2α UB−/− mice developed mild renal hypoplasia characterized by decreased ureteric branching morphogenesis but maintained normal overall branching architecture and had normal mesenchymal stromal development. Reduced nephron endowment in postnatal mutant mice was observed, corresponding with the reduction in branching morphogenesis. Furthermore, there were no apparent renal abnormalities in Fgfr2 LR/LR mice. Interestingly, Etv4 and Etv5 expression was unaltered in Frs2α UB−/− mice, as was Sprouty1, an antagonist of Frs2α signaling. However, Ret and Wnt11 (molecules critical for ureteric branching morphogenesis) mRNA levels were lower in mutants vs. controls. Taken together, these findings suggest that Fgfr2 signals through adapter molecules other than Frs2α in the ureteric epithelium. Furthermore, Frs2α may transmit signals through other receptor kinases present in ureteric epithelium. Finally, the renal hypoplasia observed in Frs2α UB−/− mice is likely secondary to decreased Ret and Wnt11 expression.

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24

Wang, Jian-Jiang, Yue-Xin Liu, Wei Wang, Wei Yan, Yu-Peng Zheng, Lu-Dong Qiao, Dan Liu, and Shan Chen. "Fusion Between TMPRSS2 and ETS Family Members (ERG, ETV1, ETV4) in Prostate Cancers from Northern China." Asian Pacific Journal of Cancer Prevention 13, no. 10 (October 31, 2012): 4935–38. http://dx.doi.org/10.7314/apjcp.2012.13.10.4935.

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25

Herriges, John, and Xin Sun. "Investigating the role of FGF-regulated transcription factors ETV4 and ETV5 in lung development and maturation." Developmental Biology 356, no. 1 (August 2011): 251. http://dx.doi.org/10.1016/j.ydbio.2011.05.561.

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26

Neri, Paola, Ines Tagoug, Ranjan Maity, Caleb K. Stein, Madison Kong, Jonathan Keats, David Soong, Christopher Chiu, P. Leif Bergsagel, and Nizar J. Bahlis. "Transcriptional Plasticity Compensates for Ikaros and Aiolos Proteasomal Degradation and Mediates Resistance to IMiDs in Multiple Myeloma (MM)." Blood 130, Suppl_1 (December 7, 2017): 63. http://dx.doi.org/10.1182/blood.v130.suppl_1.63.63.

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Abstract Background: Immunoglobulin (IGH, IGL, IGK) and non-immunoglobulin (PVT1, TXNDC5, FAM46C, DUSP22, etc.) enhancers hijacking by variable genes (MYC, MAF, MAFB, CCND1/2/3, MMSET, IRF4) is a recognized oncogenic driver event in MM. However, the identity of the transcription factors (TFs) or transcriptional regulatory complexes binding and regulating the activity of these enhancers remains to be fully elucidated and may yield valuable therapeutic targets. As such the discovery of the BET family member BRD4 as the master histone acetyl mark reader at enhancers loci regulating MYC lead to promising therapeutic developments in MM and numerous other cancers. Immunomodulatory drugs (IMiDs) promote the proteasomal degradation of IKAROS (IKZF1) and AIOLOs (IKZF3) leading to the transcriptional repression of MYC and the suppression of MM cells survival and proliferation. However, acquired resistance to IMIDs and the loss of the transcriptional repression of MYC are nearly universal and occur in spite of sustained IKZF1/3 degradation suggesting that transcriptional rewiring may be sustaining hijacked enhancers activity and transcription of driver oncogenes. Methods and Results: In order to define how IMiDs repress MYC transcription, we first defined IKZF1, BRD4, the lysine acetyl transferase P300 and the mediator complex subunit MED1 mapping within the MM genome using ChIPseq. In MM cell lines (MM1S, RPMI8226, ARP1 and AMO1), IKZF1 predominantly mapped to intronic and intergenic loci which are typically enriched with enhancer and superenhancer elements. Indeed, IKZF1 mapping to the genome nearly completely (96.5%) overlapped that of P300, MED1 and BRD4 co-occupied enhancer and superenhancer loci. We also confirmed that in the MM1S sensitive cell lines IMiDs (lenalidomide 10 μM, 24h) exposure efficiently depleted IKZF1, BRD4, P300 and MED1 at enhancer loci with ensuing MYC (and MAF) downregulation. In contrast, in resistant cell lines (RPMI8226) and in spite efficient IKZF1 displacement, BRD4, P300 and MED1 were retained at the oncogenic enhancer (IGLL5) driving MYC (and MAF). These findings lead us to postulate that in IMiDs resistant cells retention of BRD4 and MED1 at oncogenic enhancers in the absence of IKZF1 likely results from rewiring of the TFs regulating MYC. To identify TFs that may co-localize with BRD4 and IKZF1, we analyzed the enrichment of DNA motifs at IKZF1and BRD4 co-occupied enhancers using the MEME suite motif-finding algorithms. This computational analysis revealed a strong enrichment at these MM enhancers of the GGAA motif recognized by the ETS family of TFs (P= 3.2 e-743) and other motifs boxes for the RUNX (P= 9.6 e-725), MYC/MYB ( P= 8.8 e-52) and interferon regulatory (IRF) (P= 3.1 e-293) TFs. We next confirmed that the ETS family TF ETV4 was indeed expressed in IMiDs resistant, but not sensitive, MM cell lines. ChiPseq occupancy profiles in IMiDs resistant RPMI8226 cell line revealed co-localization of ETV4 with IKZF1, P300 and BRD4. As predicted, lenalidomide treatment induced global depletion of IKZF1 but not ETV4 at BRD4 occupied enhancers in resistant cell lines (RPMI8226 and ARP1). Importantly, Cas9-mediated knock out of ETV4 in RPMI8226 cells sensitized them to lenalidomide with ensuing MYC downregulation and cell death. Confirming its role in MM, ETV4 transcript was indeed detectable in primary patients' samples in the CoMMpass data repository (ETV4 FPKM >1.0 in 112/724) and its expression was associated with significantly reduced survival outcomes (HR 0.64; P=0.0008). Similarly, high expression (top quartiles) of RUNX2 or MYB, TFs with enriched motifs at IKZF1 co-occupied enhancer loci, was also associated with decreased survival. Of note RNAseq analysis of paired patient samples pre- and post-IMiDs treatment (n=14 pairs) revealed significant upregulation of ETV4 at the time of acquired IMiDs resistance (7/14). Lastly transcriptome analysis of 101 patients enrolled in the RD arm (lenalidomide and dexamethasone) of the POLLUX trial (NCT02076009) confirmed the reduced survival of patients with top quartiles expression of ETV4 as well as MYB and RUNX2 (Fig.1) Conclusion: Transcriptional plasticity with expression of extra-lineage TFs such as the ETS family member ETV4 sustains oncogenic enhancers in MM overcoming IKAROS and AIOLOS dependency and promoting IMiDs resistance. Figure 1 Figure 1. Disclosures Neri: Celgene: Consultancy, Honoraria, Research Funding; Janssen: Consultancy, Honoraria, Research Funding. Soong: Jannsen: Employment. Chiu: Janssen: Employment. Bahlis: Takeda: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees; Amgen: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Janssen: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Celgene: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau.

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Schafer, Cara, Denise Young, Yingjie Song, Jiji Jiang, Albert Dobi, Gyorgy Petrovics, Bettina F. Drake, Gregory T. Chesnut, Isabell A. Sesterhenn, and Shyh-Han Tan. "Abstract 2220: Immunohistochemical detection of prostate cancer heterogeneity by using ETS and PTEN monoclonal antibodies." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2220. http://dx.doi.org/10.1158/1538-7445.am2022-2220.

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Abstract The multifocality and highly variable molecular pathology of prostate cancer are underlying features of this clinically heterogeneous disease. Most patients harbor multiple molecularly distinct cancer foci at diagnosis that likely arose as independent clones. There is a critical need for molecular biomarkers that can distinguish the multifocality and inter-focal heterogeneity of tumors and help stratify patients for treatment. PTEN loss and ETS gene rearrangements are among the most prevalent genomic alterations in prostate carcinogenesis. The detection of both ERG overexpression and PTEN protein loss by immunohistochemistry (IHC) have proven to be reliable substitutes for detecting genomic alterations by fluorescence in situ hybridization (FISH) assay. We developed monoclonal antibodies against ETV1 and ETV4 and evaluated their performance in prostate cancer specimens. The expression of ETV1, ETV4, were examined in relation to ERG and loss of PTEN expression in TMAs constructed from primary prostate cancer specimens of two independent patient cohorts. The first TMA was constructed from multiple 1 mm cores representing distinct tumor focus from multifocal tumors from 50 African American (AA) and 50 Caucasian American (CA) men. The second was constructed from a single 2 mm core of individual tumors from an independent cohort of 152 AA and 304 CA men. We present results on the expression of each protein biomarker in the context of patient race and their association with clinico-pathologic features, together with concurrence or mutual exclusiveness for each event. These results support the application of ETS monoclonal antibodies in IHC assays to detect prostate cancer tumor heterogeneity and to identify subsets of prostate cancer. Citation Format: Cara Schafer, Denise Young, Yingjie Song, Jiji Jiang, Albert Dobi, Gyorgy Petrovics, Bettina F. Drake, Gregory T. Chesnut, Isabell A. Sesterhenn, Shyh-Han Tan. Immunohistochemical detection of prostate cancer heterogeneity by using ETS and PTEN monoclonal antibodies [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2220.

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Gupta, Avinash, Christopher Towers, Frances Willenbrock, Roz Brant, Darren Richard Hodgson, Alan Sharpe, Paul Smith, et al. "Dual-specificity protein phosphatase DUSP4 regulates response to MEK inhibition in BRAF wild-type melanoma." British Journal of Cancer 122, no. 4 (December 16, 2019): 506–16. http://dx.doi.org/10.1038/s41416-019-0673-5.

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Abstract Background Aiming to improve treatment options for BRAF wild-type melanoma, we previously conducted the DOC-MEK study of docetaxel with MEK inhibitor (MEKi) selumetinib or placebo, revealing trends to prolongation of progression-free survival (hazard ratio 0.75, P = 0.130), and improved response rates (32% vs 14%, P = 0.059) with docetaxel plus selumetinib. NRAS status did not associate with outcome. Here, the aim was to identify novel biomarkers of response to MEKi. Methods A MEK 6 gene signature was quantified using NanoString and correlated with clinical outcomes. Two components of the gene signature were investigated by gene silencing in BRAF/NRAS wild-type melanoma cells. Results In melanomas of patients on the selumetinib but not the placebo arm, two gene signature components, dual-specificity protein phosphatase 4 (DUSP4) and ETS translocation variant 4 (ETV4), were expressed more highly in responders than non-responders. In vitro, ETV4 depletion inhibited cell survival but did not influence sensitivity to MEKi selumetinib or trametinib. In contrast, DUSP4-depleted cells showed enhanced cell survival and increased resistance to both selumetinib and trametinib. Conclusions ETV4 and DUSP4 associated with clinical response to docetaxel plus selumetinib. DUSP4 depletion induced MEKi resistance, suggesting that DUSP4 is not only a biomarker but also a mediator of MEKi sensitivity. Clinical Trial Registration DOC-MEK (EudraCT no: 2009-018153-23).

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Kuure, S., X. Chi, B. Lu, and F. Costantini. "The transcription factors Etv4 and Etv5 mediate formation of the ureteric bud tip domain during kidney development." Development 137, no. 12 (May 12, 2010): 1975–79. http://dx.doi.org/10.1242/dev.051656.

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Song, Young Shin, Seong-Keun Yoo, Hwan Hee Kim, Gyeongseo Jung, Ah-Reum Oh, Ji-Young Cha, Su-jin Kim, et al. "Interaction of BRAF-induced ETS factors with mutant TERT promoter in papillary thyroid cancer." Endocrine-Related Cancer 26, no. 6 (June 2019): 629–41. http://dx.doi.org/10.1530/erc-17-0562.

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Synergistic effects of BRAFV600E and TERT promoter mutations on the poor clinical outcomes in papillary thyroid cancer (PTC) have been demonstrated. The potential mechanism of this phenomenon has been proposed: MAPK pathway activation by the BRAFV600E mutation may upregulate E-twenty six (ETS) transcription factors, increasing TERT expression by binding to the ETS-binding site generated by the TERT promoter mutation; however, it has not yet been fully proven. This article provides transcriptomic insights into the interaction between BRAFV600E and TERT promoter mutations mediated by ETS factors in PTC. RNA sequencing data on 266 PTCs from The Cancer Genome Atlas and 65 PTCs from our institute were analyzed for gene expression changes and related molecular pathways, and the results of transcriptomic analyses were validated by in vitro experiments. TERT mRNA expression was increased by the coexistence of BRAFV600E and TERT promoter mutations (fold change, 16.17; q-value = 7.35 × 10−12 vs no mutation). In the ETS family of transcription factors, ETV1, ETV4 and ETV5 were upregulated by the BRAFV600E/MAPK pathway activation. These BRAFV600E-induced ETS factors selectively bound to the mutant TERT promoter. The molecular pathways activated by BRAFV600E were further augmented by adding the TERT promoter mutation, and the pathways related to immune responses or adhesion molecules were upregulated by TERT expression. The mechanism of the synergistic effect between BRAFV600E and TERT promoter mutations on cancer invasiveness and progression in PTC may be explained by increased TERT expression, which may result from the BRAF-induced upregulation of several ETS transcription factors.

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Mesquita, Diana, João D. Barros-Silva, Joana Santos, Rolf I. Skotheim, Ragnhild A. Lothe, Paula Paulo, and Manuel R. Teixeira. "Specific and redundant activities of ETV1 and ETV4 in prostate cancer aggressiveness revealed by co-overexpression cellular contexts." Oncotarget 6, no. 7 (February 14, 2015): 5217–36. http://dx.doi.org/10.18632/oncotarget.2847.

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Euhus, David, Dawei Bu, Xian-Jin Xie, Venetia Sarode, Raheela Ashfaq, Kelly Hunt, Weiya Xia, et al. "Tamoxifen Downregulates Ets Oncogene Family Members ETV4 and ETV5 in Benign Breast Tissue: Implications for Durable Risk Reduction." Cancer Prevention Research 4, no. 11 (July 21, 2011): 1852–62. http://dx.doi.org/10.1158/1940-6207.capr-11-0186.

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Krishnan, Moorthy, Lynne A. Lapierre, Byron C. Knowles, and James R. Goldenring. "Rab25 regulates integrin expression in polarized colonic epithelial cells." Molecular Biology of the Cell 24, no. 6 (March 15, 2013): 818–31. http://dx.doi.org/10.1091/mbc.e12-10-0745.

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Rab25 is a tumor suppressor for colon cancer in humans and mice. To identify elements of intestinal polarity regulated by Rab25, we developed Caco2-BBE cell lines stably expressing short hairpin RNA for Rab25 and lines rescuing Rab25 knockdown with reexpression of rabbit Rab25. Rab25 knockdown decreased α2-, α5-, and β1-integrin expression. We observed colocalization and direct association of Rab25 with α5β1-integrins. Rab25 knockdown also up-regulated claudin-1 expression, increased transepithelial resistance, and increased invasive behavior. Rab25-knockdown cells showed disorganized brush border microvilli with decreases in villin expression. All of these changes were reversed by reintroduction of rabbit Rab25. Rab25 knockdown altered the expression of 29 gene transcripts, including the loss of α5-integrin transcripts. Rab25 loss decreased expression of one transcription factor, ETV4, and overexpression of ETV4 in Rab25-knockdown cells reversed losses of α5β1-integrin. The results suggest that Rab25 controls intestinal cell polarity through the regulation of gene expression.

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Fei, Xinfeng, Yuying Cai, Feng Lin, Yongyi Huang, Te Liu, and Yan Liu. "Amniotic fluid mesenchymal stem cells repair mouse corneal cold injury by promoting mRNA N4-acetylcytidine modification and ETV4/JUN/CCND2 signal axis activation." Human Cell 34, no. 1 (October 3, 2020): 86–98. http://dx.doi.org/10.1007/s13577-020-00442-7.

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AbstractSevere corneal injury is one of the main causes of loss of visual function. Mesenchymal stem cells (MSCs) have the ability to repair damaged cells in vivo. The present study aimed to explore whether MSCs could function as a cell therapy tool to replace traditional methods to treat corneal injury. CD44 + /CD105 + mesenchymal stem cells isolated from mouse amniotic fluid (mAF-MSCs) were injected into mice after cryoinjury to induce corneal endothelial cell injury. Histopathological assays indicated that mAF-MSCs could promote the growth of corneal epithelial cells, reduce keratitis, and repair the corneal damage caused by low temperature. cDNA microarray analysis revealed that the mAF-MSCs affected the expression patterns of mRNAs related to cell proliferation and differentiation pathways in the mice after transplantation. The results of quantitative real-time PCR and western blotting revealed that NAT12, NAT10, and the ETV4/JUN/CCND2 signaling axis were elevated significantly in the mAF-MSC-transplantation group, compared with those in the phosphate-buffered saline-treated groups. High performance liquid chromatography–mass spectroscopy results revealed that mAF-MSCs could promote mRNA N4-acetylcytidine (ac4C) modification and high expression of N-acetyltransferase in the eyeballs. RNA immunoprecipitation-PCR results showed that a specific product comprising Vegfa, Klf4, Ccnd2, Jun, and Etv4 mRNA specific coding region sites could be amplified using PCR from complexes formed in mAF-MSC-transplanted samples cross-linked with anti-ac4C antibodies. Thus, mouse amniotic fluid MSCs could repair the mouse corneal cold injury by promoting the ETV4/JUN/CCND2 signal axis activation and improving its stability by stimulating N4-acetylcytidine modification of their mRNAs.

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Zhang, Xueming, Yang Liu, Guanyu Che, Yixue Sun, Bo Jin, and Bin Guo. "Expression of Etv4 mRNA in Cryptorchidism Mouse Testis and Epididymis." Journal of Animal and Veterinary Advances 11, no. 12 (December 1, 2012): 2163–65. http://dx.doi.org/10.3923/javaa.2012.2163.2165.

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Wu, Yung-Fu, Chih-Yang Wang, Wan-Chun Tang, Yu-Cheng Lee, Hoang Dang Khoa Ta, Li-Chia Lin, Syu-Ruei Pan, Yi-Chun Ni, Gangga Anuraga, and Kuen-Haur Lee. "Expression Profile and Prognostic Value of Wnt Signaling Pathway Molecules in Colorectal Cancer." Biomedicines 9, no. 10 (September 27, 2021): 1331. http://dx.doi.org/10.3390/biomedicines9101331.

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Colorectal cancer (CRC) is a heterogeneous disease with changes in the genetic and epigenetic levels of various genes. The molecular assessment of CRC is gaining increasing attention, and furthermore, there is an increase in biomarker use for disease prognostication. Therefore, the identification of different gene biomarkers through messenger RNA (mRNA) abundance levels may be useful for capturing the complex effects of CRC. In this study, we demonstrate that the high mRNA levels of 10 upregulated genes (DPEP1, KRT80, FABP6, NKD2, FOXQ1, CEMIP, ETV4, TESC, FUT1, and GAS2) are observed in CRC cell lines and public CRC datasets. Moreover, we find that a high mRNA expression of DPEP1, NKD2, CEMIP, ETV4, TESC, or FUT1 is significantly correlated with a worse prognosis in CRC patients. Further investigation reveals that CTNNB1 is the key factor in the interaction of the canonical Wnt signaling pathway with 10 upregulated CRC-associated genes. In particular, we identify NKD2, FOXQ1, and CEMIP as three CTNNB1-regulated genes. Moreover, individual inhibition of the expression of three CTNNB1-regulated genes can cause the growth inhibition of CRC cells. This study reveals efficient biomarkers for the prognosis of CRC and provides a new molecular interaction network for CRC.

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Kim, Eunjeong, Donghyo Kim, Jeon-Soo Lee, Jeehyun Yoe, Jongmin Park, Chang-Jin Kim, Dongjun Jeong, Sanguk Kim, and Yoontae Lee. "Capicua suppresses hepatocellular carcinoma progression by controlling the ETV4-MMP1 axis." Hepatology 67, no. 6 (April 19, 2018): 2287–301. http://dx.doi.org/10.1002/hep.29738.

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Fontanet, P., D. Irala, F. C. Alsina, G. Paratcha, and F. Ledda. "Pea3 Transcription Factor Family Members Etv4 and Etv5 Mediate Retrograde Signaling and Axonal Growth of DRG Sensory Neurons in Response to NGF." Journal of Neuroscience 33, no. 40 (October 2, 2013): 15940–51. http://dx.doi.org/10.1523/jneurosci.0928-13.2013.

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Akagi, Tadayuki, Satu Kuure, Kousuke Uranishi, Hiroshi Koide, Frank Costantini, and Takashi Yokota. "ETS-related Transcription Factors ETV4 and ETV5 Are Involved in Proliferation and Induction of Differentiation-associated Genes in Embryonic Stem (ES) Cells." Journal of Biological Chemistry 290, no. 37 (July 29, 2015): 22460–73. http://dx.doi.org/10.1074/jbc.m115.675595.

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Lu, Zhichun, Sean R. Williamson, Shannon Carskadon, Pavithra D. Arachchige, Gaury Dhamdhere, Daniel S. Schultz, Hans Stricker, et al. "Clonal evaluation of early onset prostate cancer by expression profiling of ERG, SPINK1, ETV1 , and ETV4 on whole‐mount radical prostatectomy tissue." Prostate 80, no. 1 (October 4, 2019): 38–50. http://dx.doi.org/10.1002/pros.23914.

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Tomlins, Scott A., Rohit Mehra, Daniel R. Rhodes, Lisa R. Smith, Diane Roulston, Beth E. Helgeson, Xuhong Cao, et al. "TMPRSS2:ETV4 Gene Fusions Define a Third Molecular Subtype of Prostate Cancer." Cancer Research 66, no. 7 (April 1, 2006): 3396–400. http://dx.doi.org/10.1158/0008-5472.can-06-0168.

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Rodriguez, Adriana C., Jeffery M. Vahrenkamp, Kristofer C. Berrett, Kathleen A. Clark, Katrin P. Guillen, Sandra D. Scherer, Chieh-Hsiang Yang, et al. "ETV4 Is Necessary for Estrogen Signaling and Growth in Endometrial Cancer Cells." Cancer Research 80, no. 6 (February 11, 2020): 1234–45. http://dx.doi.org/10.1158/0008-5472.can-19-1382.

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Kibel, Adam S. "TMPRSS2:ETV4 gene fusions define a third molecular subtype of prostate cancer." Urologic Oncology: Seminars and Original Investigations 25, no. 5 (September 2007): 448. http://dx.doi.org/10.1016/j.urolonc.2007.07.003.

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Moss, Alan C., Garrett Lawlor, David Murray, Dónal Tighe, Stephen F. Madden, Anne-Marie Mulligan, Conor O. Keane, Hugh R. Brady, Peter P. Doran, and Padraic MacMathuna. "ETV4 and Myeov knockdown impairs colon cancer cell line proliferation and invasion." Biochemical and Biophysical Research Communications 345, no. 1 (June 2006): 216–21. http://dx.doi.org/10.1016/j.bbrc.2006.04.094.

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Cheng, Tingting, Zijian Zhang, Yuyu Cheng, Jing Zhang, Jianbing Tang, Zhaohua Tan, Zhan Liang, et al. "ETV4 promotes proliferation and invasion of lung adenocarcinoma by transcriptionally upregulating MSI2." Biochemical and Biophysical Research Communications 516, no. 1 (August 2019): 278–84. http://dx.doi.org/10.1016/j.bbrc.2019.06.115.

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Khosh Kish, Ealia, Yaser Gamallat, Muhammad Choudhry, Sunita Ghosh, Sima Seyedi, and Tarek A. Bismar. "Glycyl-tRNA Synthetase (GARS) Expression Is Associated with Prostate Cancer Progression and Its Inhibition Decreases Migration, and Invasion In Vitro." International Journal of Molecular Sciences 24, no. 5 (February 21, 2023): 4260. http://dx.doi.org/10.3390/ijms24054260.

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Glycyl-tRNA synthetase (GARS) is a potential oncogene associated with poor overall survival in various cancers. However, its role in prostate cancer (PCa) has not been investigated. Protein expression of GARS was investigated in benign, incidental, advanced, and castrate-resistant PCa (CRPC) patient samples. We also investigated the role of GARS in vitro and validated GARS clinical outcomes and its underlying mechanism, utilizing The Cancer Genome Atlas Prostate Adenocarcinoma (TCGA PRAD) database. Our data revealed a significant association between GARS protein expression and Gleason groups. Knockdown of GARS in PC3 cell lines attenuated cell migration and invasion and resulted in early apoptosis signs and cellular arrest in S phase. Bioinformatically, higher GARS expression was observed in TCGA PRAD cohort, and there was significant association with higher Gleason groups, pathological stage, and lymph nodes metastasis. High GARS expression was also significantly correlated with high-risk genomic aberrations such as PTEN, TP53, FXA1, IDH1, SPOP mutations, and ERG, ETV1, and ETV4 gene fusions. Gene Set Enrichment Analysis (GSEA) of GARS through the TCGA PRAD database provided evidence for upregulation of biological processes such as cellular proliferation. Our findings support the oncogenic role of GARS involved in cellular proliferation and poor clinical outcome and provide further evidence for its use as a potential biomarker in PCa.

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I.V, Ambily Nath, and Achuthsankar S. Nair. "Bioinformatics screening of ETV4 transcription factor oncogenes and identifying small‐molecular anticancer drugs." Chemical Biology & Drug Design 99, no. 2 (November 22, 2021): 277–85. http://dx.doi.org/10.1111/cbdd.13981.

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Zhang, Xueming, Guanyu Che, Yang Liu, Yixue Sun, and Bin Guo. "Expression of ETS Transcription Factor Etv4 in Busulfan-Treated Mouse Testis and Epididymis." Journal of Animal and Veterinary Advances 11, no. 15 (December 1, 2012): 2801–3. http://dx.doi.org/10.3923/javaa.2012.2801.2803.

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Wollenick, Kristin, Jun Hu, Glen Kristiansen, Peter Schraml, Hubert Rehrauer, Utta Berchner-Pfannschmidt, Joachim Fandrey, Roland H. Wenger, and Daniel P. Stiehl. "Synthetic transactivation screening reveals ETV4 as broad coactivator of hypoxia-inducible factor signaling." Nucleic Acids Research 40, no. 5 (November 9, 2011): 1928–43. http://dx.doi.org/10.1093/nar/gkr978.

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Keenan, Melissa M., Beiyu Liu, Xiaohu Tang, Jianli Wu, Derek Cyr, Robert D. Stevens, Olga Ilkayeva, et al. "ACLY and ACC1 Regulate Hypoxia-Induced Apoptosis by Modulating ETV4 via α-ketoglutarate." PLOS Genetics 11, no. 10 (October 9, 2015): e1005599. http://dx.doi.org/10.1371/journal.pgen.1005599.

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