Research progression of slit guidance ligand 3

doi:10.3969/j.issn.1006-7795.2024.05.026

Abstract

Abstract: Slit guidance ligand (Slit) is a family of highly conserved secreted glycoproteins that interact with their roundabout guidance receptor (Robo). At present, three Slit genes (Slit 1-3) and four Robo genes (Robo 1-4) have been identified in mammals. Studies have shown that Slit3 has a wide range of biological functions, such as cell migration, bone formation, angiogenesis, and tumorigenesis. At the same time, the mechanisms of Slit3-involved diseases have been investigated, though the pathogenesis of Slit3 is not fully understood. Through studying the pathogenesis of Slit3, we could better explore the pathogenic targets for disease progression and specific treatment. This review summarized the research progress of Slit3 in various diseases, and expounded its role and possible mechanism in related diseases.

Key words: Slit3, pathogenesis, research progression

CLC Number:

R363

Jiang Huan , Li Jiaoqing, Xu Haosen , Lan Jinyi , Yang Shanzhi , Zhang Ting , Liu Peimin , Wu Danfeng , Bai Xiaoyan. Research progression of slit guidance ligand 3[J]. Journal of Capital Medical University, 2024, 45(5): 917-922.

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URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2024.05.026

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2024/V45/I5/917

References

［1］Jürgens G, Wieschaus E, Nüsslein-Volhard C, et al. Mutations affecting the pattern of the larval cuticle inDrosophila melanogaster : Ⅱ. Zygotic loci on the third chromosome［J］. Wilehm Roux Arch Dev Biol, 1984, 193(5): 283－295.
［2］Rothberg J M, Hartley D A, Walther Z, et al. Slit: an EGF-homologous locus of D. melanogaster involved in the development of the embryonic central nervous system［J］. Cell, 1988, 55(6): 1047－1059.
［3］Ypsilanti A R, Zagar Y, Chédotal A. Moving away from the midline: new developments for Slit and Robo［J］. Development, 2010, 137(12): 1939－1952.
［4］Blockus H, Chédotal A. Slit-Robo signaling［J］. Development, 2016, 143(17): 3037－3044.
［5］Katoh Y, Katoh M. Comparative genomics on SLIT1, SLIT2, and SLIT3 orthologs［J］. Oncol Rep, 2005, 14(5): 1351－1355.
［6］Tanno T, Fujiwara A, Sakaguchi K, et al. Slit3 regulates cell motility through Rac/Cdc42 activation in lipopolysaccharide-stimulated macrophages［J］. FEBS Lett, 2007, 581(5): 1022－1026.
［7］Zhang B, Dietrich U M, Geng J G, et al. Repulsive axon guidance molecule Slit3 is a novel angiogenic factor［J］. Blood, 2009, 114(19): 4300－4309.
［8］Kim B J, Lee Y S, Lee S Y, et al. Osteoclast-secreted Slit3 coordinates bone resorption and formation［J］. J Clin Invest, 2018, 128(4): 1429－1441.
［9］Dickinson R E, Dallol A, Bieche I, et al. Epigenetic inactivation of SLIT3 and SLIT1 genes in human cancers［J］. Br J Cancer, 2004, 91(12): 2071－2078.
［10］Zhao J J, Bruche S, Potts H G, et al. Tissue-Specific roles for the Slit-Robo pathway during heart, caval vein, and diaphragm development［J］. J Am Heart Assoc, 2022, 11(7): e023348.
［11］Tong M F, Jun T, Nie Y Z, et al. The role of the slit/Robo signaling pathway［J］. J Cancer, 2019, 10(12): 2694－2705.
［12］Howitt J A, Clout N J, Hohenester E. Binding site for Robo receptors revealed by dissection of the leucine-rich repeat region of Slit［J］. EMBO J, 2004, 23(22): 4406－4412.
［13］Liu J M, Zhang L, Wang D M, et al. Congenital diaphragmatic hernia, kidney agenesis and cardiac defects associated with Slit3-deficiency in mice［J］. Mech Dev, 2003, 120(9): 1059－1070.
［14］Geutskens S B, Andrews W D, van Stalborch A M D, et al. Control of human hematopoietic stem/progenitor cell migration by the extracellular matrix protein Slit3［J］. Lab Invest, 2012, 92(8): 1129－1139.
［15］Geutskens S B, Hordijk P L. Van hennik P B. The chemorepellent slit3 promotes monocyte migration［J］. J Immunol, 2010, 185(12): 7691－7698.
［16］Little M H, Wilkinson L, Brown D L, et al. Dual trafficking of Slit3 to mitochondria and cell surface demonstrates novel localization for Slit protein［J］. Am J Physiol Cell Physiol, 2001, 281(2): C486-C495.
［17］Jiang L Y, Sun J X, Huang D M. Role of slit/Robo signaling pathway in bone metabolism［J］. Int J Biol Sci, 2022, 18(3): 1303－1312.
［18］Li N, Inoue K, Sun J, et al. Osteoclasts are not a source of SLIT3［J］. Bone Research, 2020, 8(1): 11.
［19］Peng Y, Wu S, Li Y S, et al. Type H blood vessels in bone modeling and remodeling［J］. Theranostics, 2020, 10(1): 426－436.
［20］Xu R, Yallowitz A, Qin A, et al. Targeting skeletal endothelium to ameliorate bone loss［J］. Nat Med, 2018, 24(6): 823－833.
［21］Tian S, Zou Y X, Wang J, et al. Protective effect of Du-Zhong-Wan against osteoporotic fracture by targeting the osteoblastogenesis and angiogenesis couple factor SLIT3［J］. J Ethnopharmacol, 2022, 295: 115399.
［22］Tang Y, Cai J X, Lv B. LncRNA ubiquitin-binding protein domain protein 10 antisense RNA 1 inhibits colon adenocarcinoma progression via the miR-515-5p/slit guidance ligand 3 axis［J］. Bioengineered, 2022, 13(2): 2308－2320.
［23］Ng L, Chow A K M, Man J H W, et al. Suppression of slit3 induces tumor proliferation and chemoresistance in hepatocellular carcinoma through activation of GSK3β/β-catenin pathway［J］. BMC Cancer, 2018, 18(1): 621.
［24］Dammann R, Strunnikova M, Schagdarsurengin U, et al. CpG island methylation and expression of tumour-associated genes in lung carcinoma［J］. Eur J Cancer, 2005, 41(8): 1223－1236.
［25］Wang J, Yu X F, OUYang N, et al. Multi-platform analysis of methylation-regulated genes in human lung adenocarcinoma［J］. J Toxicol Environ Health A, 2019, 82(1): 37－45.
［26］Zhang C, Guo H, Li B, et al. Effects of slit3 silencing on the invasive ability of lung carcinoma a549 cells［J］. Oncol Rep, 2015, 34(2): 952－960.
［27］Jabbari K, Winkelmaier G, Andersen C, et al. Protein ligands in the secretome of CD36(+)fibroblasts induce growth suppression in a subset of breast cancer cell lines［J］. Cancers (Basel), 2021, 13(18): 4521.
［28］Denk A E, Braig S, Schubert T, et al. Slit3 inhibits activator protein 1-mediated migration of malignant melanoma cells［J］. Int J Mol Med, 2011, 28(5): 721－726.
［29］Greenberg J M, Thompson F Y, Brooks S K, et al. Slit and robo expression in the developing mouse lung［J］. Dev Dyn, 2004, 230(2): 350－360.
［30］Yuan W L, Rao Y, Babiuk R P, et al. A genetic model for a central (septum transversum) congenital diaphragmatic hernia in mice lacking Slit3［J］. Proc Natl Acad Sci USA, 2003, 100(9): 5217－5222.
［31］Piper M, Georgas K, Yamada T, et al. Expression of the vertebrate Slit gene family and their putative receptors, the Robo genes, in the developing murine kidney［J］. Mech Dev, 2000, 94(1/2): 213－217.
［32］Sanna-Cherchi S, Khan K, Westland R, et al. Exome-wide Association Study Identifies GREB1L Mutations in Congenital Kidney Malformations［J］. Am J Hum Genet, 2017, 101(5): 789－802.
［33］Zambrano S, He L Q, Kano T, et al. Molecular insights into the early stage of glomerular injury in IgA nephropathy using single-cell RNA sequencing［J］. Kidney Int, 2022, 101(4): 752－765.
［34］Zhang X Q, Chao P, Zhang L, et al. Single-cell RNA and transcriptome sequencing profiles identify immune-associated key genes in the development of diabetic kidney disease［J］. Front Immunol, 2023, 14: 1030198.
［35］Lee P S, Poh K K. Endothelial progenitor cells in cardiovascular diseases［J］. World J Stem Cells, 2014, 6(3): 355－366.
［36］Dou C J, Wang H X, Zhou G, et al. Slit3 regulates migration of endothelial progenitor cells by activation of the RhoA/Rho kinase pathway［J］. Int J Clin Exp Pathol, 2018, 11(7): 3398－3404.
［37］Wang X J, Liu J L, Yin W Q, et al. miR－218 expressed in endothelial progenitor cells contributes to the development and repair of the kidney microvasculature［J］. Am J Pathol, 2020, 190(3): 642－659.
［38］Cho H J, Kim H, Lee Y S, et al. SLIT3 promotes myogenic differentiation as a novel therapeutic factor against muscle loss［J］. J Cachexia Sarcopenia Muscle, 2021, 12(6): 1724－1740.
［39］Condac E, Strachan H, Gutierrez-Sanchez G, et al. The C-terminal fragment of axon guidance molecule Slit3 binds heparin and neutralizes heparin's anticoagulant activity［J］. Glycobiology, 2012, 22(9): 1183－1192.
［40］Zhong W, Peng Y M, Yue E L, et al. Gingival crevicular fluid levels of SLIT3 are increased in periodontal disease［J］. Oral Dis, 2020, 26(1): 182－192.