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Journal articles on the topic 'Elav-like'

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Author: Grafiati

Published: 11 March 2023

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1

Mustăciosu, Cosmin Cătălin, Adela Banciu, Călin Mircea Rusu, Daniel Dumitru Banciu, Diana Savu, Mihai Radu, and Beatrice Mihaela Radu. "RNA-Binding Proteins HuB, HuC, and HuD are Distinctly Regulated in Dorsal Root Ganglia Neurons from STZ-Sensitive Compared to STZ-Resistant Diabetic Mice." International Journal of Molecular Sciences 20, no. 8 (April 22, 2019): 1965. http://dx.doi.org/10.3390/ijms20081965.

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The neuron-specific Elav-like Hu RNA-binding proteins were described to play an important role in neuronal differentiation and plasticity by ensuring the post-transcriptional control of RNAs encoding for various proteins. Although Elav-like Hu proteins alterations were reported in diabetes or neuropathy, little is known about the regulation of neuron-specific Elav-like Hu RNA-binding proteins in sensory neurons of dorsal root ganglia (DRG) due to the diabetic condition. The goal of our study was to analyze the gene and protein expression of HuB, HuC, and HuD in DRG sensory neurons in diabetes. The diabetic condition was induced in CD-1 adult male mice with single-intraperitoneal injection of streptozotocin (STZ, 150 mg/kg), and 8-weeks (advanced diabetes) after induction was quantified the Elav-like proteins expression. Based on the glycemia values, we identified two types of responses to STZ, and mice were classified in STZ-resistant (diabetic resistant, glycemia < 260 mg/dL) and STZ-sensitive (diabetic, glycemia > 260 mg/dL). Body weight measurements indicated that 8-weeks after STZ-induction of diabetes, control mice have a higher increase in body weight compared to the diabetic and diabetic resistant mice. Moreover, after 8-weeks, diabetic mice (19.52 ± 3.52 s) have longer paw withdrawal latencies in the hot-plate test than diabetic resistant (11.36 ± 1.92 s) and control (11.03 ± 1.97 s) mice, that correlates with the installation of warm hypoalgesia due to the diabetic condition. Further on, we evidenced the decrease of Elav-like gene expression in DRG neurons of diabetic mice (Elavl2, 0.68 ± 0.05 fold; Elavl3, 0.65 ± 0.01 fold; Elavl4, 0.53 ± 0.07 fold) and diabetic resistant mice (Ealvl2, 0.56 ± 0.07 fold; Elavl3, 0.32 ± 0.09 fold) compared to control mice. Interestingly, Elav-like genes have a more accentuated downregulation in diabetic resistant than in diabetic mice, although hypoalgesia was evidenced only in diabetic mice. The Elav-like gene expression changes do not always correlate with the Hu protein expression changes. To detail, HuB is upregulated and HuD is downregulated in diabetic mice, while HuB, HuC, and HuD are downregulated in diabetic resistant mice compared to control mice. To resume, we demonstrated HuD downregulation and HuB upregulation in DRG sensory neurons induced by diabetes, which might be correlated with altered post-transcriptional control of RNAs involved in the regulation of thermal hypoalgesia condition caused by the advanced diabetic neuropathy.

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2

Toba, Gakuta, Jan Qui, Sandhya P. Koushika, and Kalpana White. "Ectopic expression ofDrosophilaELAV and human HuD inDrosophilawing disc cells reveals functional distinctions and similarities." Journal of Cell Science 115, no. 11 (June 1, 2002): 2413–21. http://dx.doi.org/10.1242/jcs.115.11.2413.

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Drosophila ELAV and human HuD are two neuronal RNA binding proteins that show remarkable sequence homology, yet differ in their respective documented roles in post-transcriptional regulation. ELAV regulates neural-specific alternative splicing of specific transcripts, and HuD stabilizes specific mRNAs that are otherwise unstable due to AU-rich elements(AREs) in their 3′ untranslated region (UTR). AREs are major determinants of transcript stability in mammalian cells. The role of each of these proteins was investigated and compared, by ectopically expressing them in Drosophila imaginal wing disc cells, which lack endogenous expression of either protein. The effect of the ectopic expression of ELAV and HuD was assessed on two sets of green fluorescent protein reporter transgenes,which were all driven with a broadly expressing promoter. Each set consisted of three reporter transgenes: (1) with an uninterrupted open reading frame(ORF); (2) with a constitutively spliced intron inserted into the ORF; and (3)with the intron nASI whose splicing is regulated in neurons by ELAV,inserted into the ORF. The two sets differed from each other only in their 3′UTR: Heat-shock-protein-70Ab (Hsp70Ab) trailer with ARE-like characteristics or Actin 5C (Act5C) trailer. Our results show that:(1) both ectopically expressed ELAV and HuD can enhance expression of transgenes with the Hsp70Ab 3′UTR, but not of transgenes with Act5C 3′UTR; (2) this enhancement is accompanied by an increase in mRNA level; (3) only ELAV can induce neural-specific splicing of nASI; and (4) although HuD is localized primarily to the cytoplasm,ELAV is localized to both the cytoplasm and the nucleus.

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3

Good, P. J. "A conserved family of elav-like genes in vertebrates." Proceedings of the National Academy of Sciences 92, no. 10 (May 9, 1995): 4557–61. http://dx.doi.org/10.1073/pnas.92.10.4557.

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4

Perron, Muriel, Marie-Pierre Furrer, Maurice Wegnez, and Laurent Théodore. "Xenopus elav-like genes are differentially expressed during neurogenesis." Mechanisms of Development 84, no. 1-2 (June 1999): 139–42. http://dx.doi.org/10.1016/s0925-4773(99)00056-8.

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5

Denkert, C., W. Weichert, S. Pest, I. Koch, D. Licht, M. Köbel, A. Reles, J. Sehouli, M. Dietel, and S. Hauptmann. "Expression of the ELAV-like protein HuR in ovarian carcinoma." Pathology - Research and Practice 200, no. 4 (January 2004): 350. http://dx.doi.org/10.1016/s0344-0338(04)80751-9.

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6

Atasoy, U., J. Watson, D. Patel, and J. D. Keene. "ELAV protein HuA (HuR) can redistribute between nucleus and cytoplasm and is upregulated during serum stimulation and T cell activation." Journal of Cell Science 111, no. 21 (November 1, 1998): 3145–56. http://dx.doi.org/10.1242/jcs.111.21.3145.

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ELAV proteins are implicated in regulating the stability and translation of cytokine and growth regulatory mRNAs such as GM-CSF, IL-2, c-myc, c-fos and GLUT1 by binding to their AU-rich 3′UTRs. The tissue-specific ELAV protein HuB (aka. Hel-N1) is predominantly cytoplasmic and has been shown to stabilize GLUT1 and c-myc mRNAs and to increase their translation following ectopic expression in 3T3-L1 cells. We report that the most widely expressed mouse ELAV protein, mHuA, is predominately nuclear in cultured NIH-3T3 cells, but is localized in the cytoplasm during early G1 of the cell cycle. Therefore, much like the primarily cytoplasmic HuB, HuA becomes temporally localized in the cytoplasm where it can potentially regulate the stability or translation of bound mRNAs. Moreover, we report that stimulation of mouse spleen cells using either mitogenic or sub-mitogenic levels of anti-CD3/CD28 resulted in a dramatic increase in the level of HuA. Upregulation of HuA corresponds to previously documented increases in cytokine expression which are due to increased mRNA stability following T cell activation. Consistent with these findings, HuA was down regulated in quiescent cells and upregulated in 3T3 cells following serum stimulation. The increase of murine HuA during the cell cycle closely resembles that of cyclin B1 which peaks in G2/M. Together with our earlier studies, these data indicate that mammalian ELAV proteins function during cell growth and differentiation due in part to their effects on posttranscriptional stability and translation of multiple growth regulatory mRNAs. This supports the hypothesis that ELAV proteins can function as transacting factors which affect a default pathway of mRNA degradation involved in the expression of growth regulatory proteins.

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7

Ma, Wei-Jun, Simon Cheng, Chris Campbell, Anne Wright, and Henry Furneaux. "Cloning and Characterization of HuR, a Ubiquitously Expressed Elav-like Protein." Journal of Biological Chemistry 271, no. 14 (April 5, 1996): 8144–51. http://dx.doi.org/10.1074/jbc.271.14.8144.

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8

Chagnovich, Daniel, Barbara E. Fayos, and Susan L. Cohn. "Differential Activity of ELAV-like RNA-binding Proteins in Human Neuroblastoma." Journal of Biological Chemistry 271, no. 52 (December 27, 1996): 33587–91. http://dx.doi.org/10.1074/jbc.271.52.33587.

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9

Kasashima, K. "Complex formation of the neuron-specific ELAV-like Hu RNA-binding proteins." Nucleic Acids Research 30, no. 20 (October 15, 2002): 4519–26. http://dx.doi.org/10.1093/nar/gkf567.

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10

Jain, R. G., L. G. Andrews, K. M. McGowan, P. H. Pekala, and J. D. Keene. "Ectopic expression of Hel-N1, an RNA-binding protein, increases glucose transporter (GLUT1) expression in 3T3-L1 adipocytes." Molecular and Cellular Biology 17, no. 2 (February 1997): 954–62. http://dx.doi.org/10.1128/mcb.17.2.954.

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3T3-L1 preadipocytes ectopically expressing the mammalian RNA-binding protein Hel-N1 expressed up to 10-fold more glucose transporter (GLUT1) protein and exhibited elevated rates of basal glucose uptake. Hel-N1 is a member of the ELAV-like family of proteins associated with the induction and maintenance of differentiation in various species. ELAV proteins are known to bind in vitro to short stretches of uridylates in the 3' untranslated regions (3'UTRs) of unstable mRNAs encoding growth-regulatory proteins involved in transcription and signal transduction. GLUT1 mRNA also contains a large 3'UTR with a U-rich region that binds specifically to Hel-N1 in vitro. Analysis of the altered GLUT1 expression at the translational and posttranscriptional levels suggested a mechanism involving both mRNA stabilization and accelerated formation of translation initiation complexes. These findings are consistent with the hypothesis that the Hel-N1 family of proteins modulate gene expression at the level of mRNA in the cytoplasm.

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11

D’Alessandro, Vito, Lucia Anna Muscarella, Massimiliano Copetti, Leopoldo Zelante, Massimo Carella, and Gianluigi Vendemiale. "Molecular Detection of Neuron-Specific ELAV-Like-Positive Cells in the Peripheral Blood of Patients with Small-Cell Lung Cancer." Analytical Cellular Pathology 30, no. 4 (January 1, 2008): 291–97. http://dx.doi.org/10.1155/2008/958014.

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Background: n-ELAV (neuronal-Embryonic Lethal, Abnormal Vision)-like genes belong to a family codifying for onconeural RNA-binding proteins. Anti-Hu-antibodies (anti-Hu-Ab) are typically associated with paraneoplastic encephalomyelitis/sensory neuropathy (PEM/PSN), and low titres of anti-Hu-Ab, were found in newly diagnosed Small Cell Lung Cancer (SCLC). The aim of this study is to develop a sensitive and quantitative molecular real-time PCR assay to detect SCLC cells in peripheral blood (PB) through nELAV-like transcripts quantification.Methods: Peripheral blood samples from 25 SCLC untreated patients and 12 healthy blood donors were investigated by realtime PCR. mRNA levels for HuB (ELAV2), HuC (ELAV3) and HuD (ELAV4) were measured in peripheral blood samples with an absolute quantification method using plasmid dilutions as calibration curves.Results: A statistically significant increase in mRNA expression level was detected for HuB and HuD in SCLC patients as compared with samples from healthy blood donors. After establishing cut off values based on the level of expression in control samples, 28% of the SCLC samples were positive for HuD expression. Overall 60% of the SCLC displayed increased level of HuD or HuB transcripts.Conclusion: Our preliminary results suggest that neuron-ELAV mRNA are detectable in peripheral blood of SCLC patients using real-time quantitative PCR.

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12

Rivas-Aravena, Andrea, Pablo Ramdohr, Maricarmen Vallejos, Fernando Valiente-Echeverría, Virginie Dormoy-Raclet, Felipe Rodríguez, Karla Pino, et al. "The Elav-like protein HuR exerts translational control of viral internal ribosome entry sites." Virology 392, no. 2 (September 2009): 178–85. http://dx.doi.org/10.1016/j.virol.2009.06.050.

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13

Amadio, Marialaura, Alessia Pascale, Stefano Govoni, Erik Laurini, Sabrina Pricl, Raffaella Gaggeri, Daniela Rossi, and Simona Collina. "Identification of Peptides with ELAV-like mRNA-Stabilizing Effect: An IntegratedIn Vitro/In SilicoApproach." Chemical Biology & Drug Design 81, no. 6 (April 11, 2013): 707–14. http://dx.doi.org/10.1111/cbdd.12117.

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14

Quattrone, A., A. Pascale, X. Nogues, W. Zhao, P. Gusev, A. Pacini, and D. L. Alkon. "Posttranscriptional regulation of gene expression in learning by the neuronal ELAV-like mRNA-stabilizing proteins." Proceedings of the National Academy of Sciences 98, no. 20 (September 25, 2001): 11668–73. http://dx.doi.org/10.1073/pnas.191388398.

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15

Kasashima, Katsumi, Kazuhiro Terashima, Koichi Yamamoto, Eiji Sakashita, and Hiroshi Sakamoto. "Cytoplasmic localization is required for the mammalian ELAV-like protein HuD to induce neuronal differentiation." Genes to Cells 4, no. 11 (November 1999): 667–83. http://dx.doi.org/10.1046/j.1365-2443.1999.00292.x.

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16

Sakurai, T., T. Yamagata, K. Uchino, H. Sezutsu, T. Tamura, and R. Kanzaki. "2.P2. Molecular cloning and expression pattern of elav-like genes from silkmoth, Bombyx mori." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 148 (August 2007): S10. http://dx.doi.org/10.1016/j.cbpa.2007.06.023.

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17

Sekii, Kiyono, Willi Salvenmoser, Katrien De Mulder, Lukas Scharer, and Peter Ladurner. "Melav2, an elav-like gene, is essential for spermatid differentiation in the flatworm Macrostomum lignano." BMC Developmental Biology 9, no. 1 (2009): 62. http://dx.doi.org/10.1186/1471-213x-9-62.

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18

Casaca, Ana. "In Vivo Interaction of the Hepatitis Delta Virus Small Antigen with the ELAV-Like Protein HuR." Open Virology Journal 5, no. 1 (March 24, 2011): 12–21. http://dx.doi.org/10.2174/1874357901105010012.

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19

Wang, Dandan, Min Wang, Chang’e Hu, Ting Shuang, Yingying Zhou, and Xiaoyu Yan. "Expression of the ELAV-like protein HuR in the cytoplasm is associated with endometrial carcinoma progression." Tumor Biology 35, no. 12 (September 3, 2014): 11939–47. http://dx.doi.org/10.1007/s13277-014-2485-9.

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20

Fujita, Masaki, Taizo Kawano, Atsunori Ohta, and Hiroshi Sakamoto. "Neuronal Expression of a Caenorhabditis elegans elav-like Gene and the Effect of Its Ectopic Expression." Biochemical and Biophysical Research Communications 260, no. 3 (July 1999): 646–52. http://dx.doi.org/10.1006/bbrc.1999.0957.

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21

Ren, Yuanfei, Maowei Yang, Xindong Wang, Buxuan Xu, Zerong Xu, and Bo Su. "ELAV-like RNA binding protein 1 regulates osteogenesis in diabetic osteoporosis: Involvement of divalent metal transporter 1." Molecular and Cellular Endocrinology 546 (April 2022): 111559. http://dx.doi.org/10.1016/j.mce.2022.111559.

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22

Liao, Chuangxin, Wenli Chen, and Jinshan Wang. "MicroRNA-20a Regulates Glioma Cell Proliferation, Invasion, and Apoptosis by Targeting CUGBP Elav-Like Family Member 2." World Neurosurgery 121 (January 2019): e519-e527. http://dx.doi.org/10.1016/j.wneu.2018.09.155.

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23

Ladd, Andrea N. "CUG-BP, Elav-like family (CELF)-mediated alternative splicing regulation in the brain during health and disease." Molecular and Cellular Neuroscience 56 (September 2013): 456–64. http://dx.doi.org/10.1016/j.mcn.2012.12.003.

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24

Ince-Dunn, Gulayse, Hirotaka J. Okano, Kirk B. Jensen, Woong-Yang Park, Ru Zhong, Jernej Ule, Aldo Mele, et al. "Neuronal Elav-like (Hu) Proteins Regulate RNA Splicing and Abundance to Control Glutamate Levels and Neuronal Excitability." Neuron 75, no. 6 (September 2012): 1067–80. http://dx.doi.org/10.1016/j.neuron.2012.07.009.

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25

Clayton, Gerald H., Gail M. Perez, Roderic L. Smith, and Geoffrey C. Owens. "Expression of mRNA for the elav-like neural-specific RNA binding protein, HuD, during nervous system development." Developmental Brain Research 109, no. 2 (August 1998): 271–80. http://dx.doi.org/10.1016/s0165-3806(98)00074-1.

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26

Blech-Hermoni, Yotam, Twishasri Dasgupta, Ryan J. Coram, and Andrea N. Ladd. "Identification of Targets of CUG-BP, Elav-Like Family Member 1 (CELF1) Regulation in Embryonic Heart Muscle." PLOS ONE 11, no. 2 (February 11, 2016): e0149061. http://dx.doi.org/10.1371/journal.pone.0149061.

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27

Ma, W. J., S. Chung, and H. Furneaux. "The Elav-like proteins bind to AU-rich elements and to the poly(A) tail of mRNA." Nucleic Acids Research 25, no. 18 (September 1, 1997): 3564–69. http://dx.doi.org/10.1093/nar/25.18.3564.

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28

Leandersson, Karin, Kristian Riesbeck, and Tommy Andersson. "Wnt-5a mRNA translation is suppressed by the Elav-like protein HuR in human breast epithelial cells." Nucleic Acids Research 34, no. 14 (August 12, 2006): 3988–99. http://dx.doi.org/10.1093/nar/gkl571.

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29

Sanna, Maria Domenica, Alessandro Quattrone, and Nicoletta Galeotti. "Antidepressant-like actions by silencing of neuronal ELAV-like RNA-binding proteins HuB and HuC in a model of depression in male mice." Neuropharmacology 135 (June 2018): 444–54. http://dx.doi.org/10.1016/j.neuropharm.2018.04.001.

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30

Denkert, Carsten, Ines Koch, Nora von Keyserlingk, Aurelia Noske, Silvia Niesporek, Manfred Dietel, and Wilko Weichert. "Expression of the ELAV-like protein HuR in human colon cancer: association with tumor stage and cyclooxygenase-2." Modern Pathology 19, no. 9 (June 23, 2006): 1261–69. http://dx.doi.org/10.1038/modpathol.3800645.

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31

Zheng, C., and BJ Baum. "Including the p53 ELAV-like protein-binding site in vector cassettes enhances transgene expression in rat submandibular gland." Oral Diseases 18, no. 5 (January 18, 2012): 477–84. http://dx.doi.org/10.1111/j.1601-0825.2011.01895.x.

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32

Do, Sung-Im, Eduard Santini Araujo, Ricardo K. Kalil, Patrizia Bacchini, Franco Bertoni, K. Krishnan Unni, and Yong-Koo Park. "Expression of Embryonic Lethal Abnormal Vision (ELAV)-Like Protein HuR and Cyclooxygenase-2 (COX-2) in Ewing Sarcoma." Tumori Journal 94, no. 3 (May 2008): 347–50. http://dx.doi.org/10.1177/030089160809400310.

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33

Zhang, Cong, Guoliang Xue, Jingwang Bi, Ming Geng, Huili Chu, Yaping Guan, Jun Wang, and Baocheng Wang. "Cytoplasmic expression of the ELAV-like protein HuR as a potential prognostic marker in esophageal squamous cell carcinoma." Tumor Biology 35, no. 1 (July 20, 2013): 73–80. http://dx.doi.org/10.1007/s13277-013-1008-4.

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34

Sakai, Koichiro, Yoko Kitagawa, and Genjiro Hirose. "Analysis of the RNA Recognition Motifs of Human Neuronal ELAV-like Proteins in Binding to a Cytokine mRNA." Biochemical and Biophysical Research Communications 256, no. 2 (March 1999): 263–68. http://dx.doi.org/10.1006/bbrc.1999.0282.

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35

Fan, Ming‐Jun, Peng‐Juan He, Xue‐Yan Lin, Chun‐Run Yang, Chang‐Zhong Li, and Li‐Gang Xing. "MicroRNA ‐324‐5p affects the radiotherapy response of cervical cancer via targeting ELAV‐like RNA binding protein 1." Kaohsiung Journal of Medical Sciences 36, no. 12 (August 5, 2020): 965–72. http://dx.doi.org/10.1002/kjm2.12277.

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36

Fleming, Victoria A., Cuiyu Geng, Andrea N. Ladd, and Hua Lou. "Alternative splicing of the neurofibromatosis type 1 pre-mRNA is regulated by the muscleblind-like proteins and the CUG-BP and ELAV-like factors." BMC Molecular Biology 13, no. 1 (2012): 35. http://dx.doi.org/10.1186/1471-2199-13-35.

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37

Doller, Anke, Sebastian Schulz, Josef Pfeilschifter, and Wolfgang Eberhardt. "RNA-dependent association with myosin IIA promotes F-actin-guided trafficking of the ELAV-like protein HuR to polysomes." Nucleic Acids Research 41, no. 19 (August 6, 2013): 9152–67. http://dx.doi.org/10.1093/nar/gkt663.

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38

Amadio, Marialaura, Alessandro Quattrone, Daniel L. Alkon, Marco Racchi, Stefano Govoni, and Alessia Pascale. "P2-124 PKC and ELAV-like mRNA binding proteins: a new cascade for memory trace formation and Alzheimer's disease." Neurobiology of Aging 25 (July 2004): S260. http://dx.doi.org/10.1016/s0197-4580(04)80871-6.

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39

Zheng, Changyu, and Bruce J. Baum. "1006. Effect on Expression of Including Binding Sites for the ELAV-Like Proteins HuD and HuR in Transgene Cassettes." Molecular Therapy 13 (2006): S387—S388. http://dx.doi.org/10.1016/j.ymthe.2006.08.1100.

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40

Chung, Sangmi, Michael Eckrich, Nora Perrone-Bizzozero, Douglas T. Kohn, and Henry Furneaux. "The Elav-like Proteins Bind to a Conserved Regulatory Element in the 3′-Untranslated Region of GAP-43 mRNA." Journal of Biological Chemistry 272, no. 10 (March 7, 1997): 6593–98. http://dx.doi.org/10.1074/jbc.272.10.6593.

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41

Joseph, Benjamin, Martin Orlian, and Henry Furneaux. "p21waf1mRNA Contains a Conserved Element in Its 3′-Untranslated Region That Is Bound by the Elav-like mRNA-stabilizing Proteins." Journal of Biological Chemistry 273, no. 32 (August 7, 1998): 20511–16. http://dx.doi.org/10.1074/jbc.273.32.20511.

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42

Wang, Jun, Dali Li, Baocheng Wang, and Yun Wu. "Predictive and prognostic significance of cytoplasmic expression of ELAV-like protein HuR in invasive breast cancer treated with neoadjuvant chemotherapy." Breast Cancer Research and Treatment 141, no. 2 (September 2013): 213–24. http://dx.doi.org/10.1007/s10549-013-2679-7.

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43

Blech-Hermoni, Yotam, and Andrea N. Ladd. "Identification of transcripts regulated by CUG-BP, Elav-like family member 1 (CELF1) in primary embryonic cardiomyocytes by RNA-seq." Genomics Data 6 (December 2015): 74–76. http://dx.doi.org/10.1016/j.gdata.2015.08.014.

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44

Dasgupta, Twishasri, and Andrea N. Ladd. "The importance of CELF control: molecular and biological roles of the CUG-BP, Elav-like family of RNA-binding proteins." Wiley Interdisciplinary Reviews: RNA 3, no. 1 (August 17, 2011): 104–21. http://dx.doi.org/10.1002/wrna.107.

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45

Papatheofani, Vasiliki, Georgia Levidou, Panagiotis Sarantis, Evangelos Koustas, Michalis V. Karamouzis, Alexandros Pergaris, Gregorios Kouraklis, and Stamatios Theocharis. "HuR Protein in Hepatocellular Carcinoma: Implications in Development, Prognosis and Treatment." Biomedicines 9, no. 2 (January 27, 2021): 119. http://dx.doi.org/10.3390/biomedicines9020119.

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Hu-antigen R (HuR) is a post-transcriptional regulator that belongs to the embryonic lethal abnormal vision Drosophila-like family (ELAV). HuR regulates the stability, translation, subcellular localization, and degradation of several target mRNAs, which are implicated in carcinogenesis and could affect therapeutic options. HuR protein is consistently highly expressed in hepatocellular carcinoma (HCC) compared to the adjacent normal liver tissue and is involved in the post-transcriptional regulation of various genes implicated in liver malignant transformation. Additionally, HuR protein seems to be a putative prognosticator in HCC, predicting worse survival. This review summarizes the recent evidence regarding the role of HuR in primary liver tumors, as presented in clinical studies, in vitro experiments and in vivo animal models. In conclusion, our review supports the consistent role of HuR protein in the development, prognosis, and treatment of HCC. Additional studies are expected to expand current information and exploit its putative employment as a future candidate for more personalized treatment in these tumors.

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46

Gu, Chijiang, Mingyuan Zhang, Weiliang Sun, and Changzheng Dong. "Upregulation of miR-324-5p Inhibits Proliferation and Invasion of Colorectal Cancer Cells by Targeting ELAVL1." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 27, no. 5 (May 7, 2019): 515–24. http://dx.doi.org/10.3727/096504018x15166183598572.

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Colorectal cancer (CRC) is a common clinical cancer that remains incurable in most cases. miRNAs are reported to play a part in the development of various tumors. In the present study, we found that miR-324-5p was downregulated in CRC cells, while ELAV (embryonic lethal, abnormal vision, Drosophila)-like protein 1 (ELAVL1) showed a higher expression. miR-324-5p transfection significantly inhibited the proliferation as well as invasion in both SW620 and SW480 cells. miR-324-5p mimic transfection markedly decreased the expression of ELAVL1. Luciferase reporter gene assay confirmed that ELAVL1 is a direct target of miR-324-5p. Furthermore, cancer invasion factors uPA, uPAR, and MMP-9 were found to drop significantly in miR-324-5p-transfected groups. To conclude, our findings indicate that miR-324-5p may play a suppressive role in colorectal cell viability and invasion, at least in part, through directly targeting ELAVL1. Therefore, miR-234-5p might function as a promising candidate for CRC treatment and deserves deeper research.

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Tan, Yang, Xueqing Sun, Yizhu Xu, Bingjie Tang, Shuaiqi Xu, Dong Lu, Yan Ye, et al. "Small molecule targeting CELF1 RNA-binding activity to control HSC activation and liver fibrosis." Nucleic Acids Research 50, no. 5 (March 2, 2022): 2440–51. http://dx.doi.org/10.1093/nar/gkac139.

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Abstract CUGBP Elav-like family member 1 (CELF1), an RNA-binding protein (RBP), plays important roles in the pathogenesis of diseases such as myotonic dystrophy, liver fibrosis and cancers. However, targeting CELF1 is still a challenge, as RBPs are considered largely undruggable. Here, we discovered that compound 27 disrupted CELF1-RNA binding via structure-based virtual screening and biochemical assays. Compound 27 binds directly to CELF1 and competes with RNA for binding to CELF1. Compound 27 promotes IFN-γ secretion and suppresses TGF-β1-induced hepatic stellate cell (HSC) activation by inhibiting CELF1-mediated IFN-γ mRNA decay. In vivo, compound 27 attenuates CCl4-induced murine liver fibrosis. Furthermore, the structure-activity relationship analysis was performed and compound 841, a derivative of compound 27, was identified as a selective CELF1 inhibitor. In conclusion, targeting CELF1 RNA-binding activity with small molecules was achieved, which provides a novel strategy for treating liver fibrosis and other CELF1-mediated diseases.

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Blech-Hermoni, Yotam, Connor B. Sullivan, Michael W. Jenkins, Oliver Wessely, and Andrea N. Ladd. "CUG-BP, Elav-like family member 1 (CELF1) is required for normal myofibrillogenesis, morphogenesis, and contractile function in the embryonic heart." Developmental Dynamics 245, no. 8 (May 31, 2016): 854–73. http://dx.doi.org/10.1002/dvdy.24413.

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Han, Jian, Judith F. Knops, John W. Longshore, and Peter H. King. "Localization ofHuman elav-like Neuronal Protein 1(Hel-N1) on Chromosome 9p21 by Chromosome Microdissection Polymerase Chain Reaction and Fluorescencein SituHybridization." Genomics 36, no. 1 (August 1996): 189–91. http://dx.doi.org/10.1006/geno.1996.0444.

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Hinney, Anke, Özgür Albayrak, Jochen Antel, Anna-Lena Volckmar, Rebecca Sims, Jade Chapman, Denise Harold, et al. "Genetic variation at theCELF1(CUGBP, elav-like family member 1 gene) locus is genome-wide associated with Alzheimer's disease and obesity." American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 165, no. 4 (May 1, 2014): 283–93. http://dx.doi.org/10.1002/ajmg.b.32234.

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