Regulatory roles of insulin growth factor binding protein family in neuroblastoma cell proliferation and differentiation: Potential prognostic biomarkers and therapeutic targets for neuroblastoma

Kai Huang , LinYu Yang , Yue Ma , Shan Wang

Pediatric Discovery ›› 2024, Vol. 2 ›› Issue (3) : e68

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Pediatric Discovery ›› 2024, Vol. 2 ›› Issue (3) : e68 DOI: 10.1002/pdi3.68
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Regulatory roles of insulin growth factor binding protein family in neuroblastoma cell proliferation and differentiation: Potential prognostic biomarkers and therapeutic targets for neuroblastoma

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Abstract

Neuroblastoma (NB), as a representative of tumors of embryonic origin in children, has specific clinical features. On the one hand, a very small number of NBs may appear to regress on their own. On the other hand, highly malignant NBs can invade the surrounding blood vessels and organs and metastasize to distant bone, bone marrow, and lymph nodes in the early stages of the disease. Based on differential affinities to insulin growth factors (IGFs), insulin growth factor binding proteins (IGFBPs) are classified into two groups: IGF binding proteins (IGFBP1-6) with high-affinity and IGF low-affinity binding proteins, such as IGFBP-related proteins (IGFBP rP1-10). IGFBP are crucial regulators of the bioavailability and function of IGF in metabolic signaling and as modulators of IGF signaling, and their role in NB is gaining increasing attention. In this study, we investigate the involvement of IGFBP family members in the growth and differentiation of NB cells, as well as the potential of IGFBPs as prognostic biomarkers and therapeutic targets for human NB.

Keywords

differentiation / growth / IGFBPs family / neuroblastoma

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Kai Huang, LinYu Yang, Yue Ma, Shan Wang. Regulatory roles of insulin growth factor binding protein family in neuroblastoma cell proliferation and differentiation: Potential prognostic biomarkers and therapeutic targets for neuroblastoma. Pediatric Discovery, 2024, 2(3): e68 DOI:10.1002/pdi3.68

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References

[1]

ZeineldinM, PatelA, DyerM. Neuroblastoma: when differentiation goes awry. Neuron. 2022;110(18):2916-2928.

[2]

PonzoniM, Bachetti T, CorriasM, et al. Recent advances in the developmental origin of neuroblastoma: an overview. J Exp Clin Cancer Res. 2022;41(1):92.

[3]

BrodeurG. Spontaneous regression of neuroblastoma. Cell tissue Res. 2018;372(2):277-286.

[4]

MatthayK, MarisJ, SchleiermacherG, et al. Neuroblastoma. Nat Rev Dis Prim. 2016;2(1):16078.

[5]

ChenC, LanM. Interplay: the essential role between INSM1 and N-myc in aggressive neuroblastoma. Biology. 2022;11(10):1376.

[6]

BartolucciD, Montemurro L, RaieliS, et al. MYCN impact on high-risk neuroblastoma: from diagnosis and prognosis to targeted treatment. Cancers. 2022;14(18):4421.

[7]

MosséY, Laudenslager M, LongoL, et al. Identification of ALK as a major familial neuroblastoma predisposition gene. Nature. 2008;455(7215):930-935.

[8]

van LimptV, ChanA, SchrammA, Eggert A, VersteegR. Phox2B mutations and the Delta-Notch pathway in neuroblastoma. Cancer Lett. 2005;228(1-2):59-63.

[9]

AkterJ, KamijoT. How do telomere abnormalities regulate the biology of neuroblastoma? Biomolecules. 2021;11(8):1112.

[10]

KoneruB, LopezG, FarooqiA, et al. Telomere maintenance mechanisms define clinical outcome in high-risk neuroblastoma. Cancer Res. 2020;80(12):2663-2675.

[11]

DuanX, ZhaoQ. TERT-Mediated and ATRX-mediated telomere maintenance and neuroblastoma. J pediatr hematol/oncol. 2018;40(1):1-6.

[12]

QiuB, Matthay K. Advancing therapy for neuroblastoma. Nat Rev Clin Oncol. 2022;19(8):515-533.

[13]

JinZ, LuY, WuY, CheJ, DongX. Development of differentiation modulators and targeted agents for treating neuroblastoma. Eur J Med Chem. 2020;207:112818.

[14]

GeorgeS, ParmarV, LorenziF, et al. Novel therapeutic strategies targeting telomere maintenance mechanisms in high-risk neuroblastoma. J Exp Clin Cancer Res. 2020;39(1):78.

[15]

PeiferM, Hertwig F, RoelsF, et al. Telomerase activation by genomic rearrangements in high-risk neuroblastoma. Nature. 2015;526(7575):700-704.

[16]

CesareA, ReddelR. Alternative lengthening of telomeres: models, mechanisms and implications. Nat Rev Genet. 2010;11(5):319-330.

[17]

StainczykS, Westermann F. Neuroblastoma-Telomere maintenance, deregulated signaling transduction and beyond. Int J Cancer. 2022;150(6):903-915.

[18]

YuE, CheungN, LueN. Connecting telomere maintenance and regulation to the developmental origin and differentiation states of neuroblastoma tumor cells. J Hematol Oncol. 2022;15(1):117.

[19]

NagyZ, Seneviratne J, KanikevichM, et al. An ALYREF-MYCN coactivator complex drives neuroblastoma tumorigenesis through effects on USP3 and MYCN stability. Nat Commun. 2021;12(1):1881.

[20]

LiuC, GenY, TanimotoK, Muramatsu T, InoueJ, InazawaJ. miR-3140-3pConcurrent targeting of MAP3K3 and BRD4 by overcomes acquired resistance to BET inhibitors in neuroblastoma cells. Mol Ther Nucleic Acids. 2021;25:83-92.

[21]

HuX, LiuR, HouJ, et al. SMARCE1 promotes neuroblastoma tumorigenesis through assisting MYCN-mediated transcriptional activation. Oncogene. 2022;41(37):4295-4306.

[22]

LauraB, RaduB, PatriciaC, Andreea M. Association of image-defined risk factors with clinical, biological features and outcome in neuroblastoma. Children. 2022;9(11):1707.

[23]

ChenJ, SunM, ChenC, Jiang B, FangY. MYCNIdentification of hub genes and their correlation with infiltration of immune cells in positive neuroblastoma based on WGCNA and LASSO algorithm. Front Immunol. 2022;13:1016683.

[24]

ParkinsonL, GillenS, WoodsL, et al. The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma. Front Cell Dev Biol. 2022;10:942579.

[25]

LuF, MuB, JinG, ZhuL, MuP. MYCN directly targets NeuroD1 to promote cellular proliferation in neuroblastoma. Oncol Res. 2022;29(1):1-10.

[26]

WestermarkU, Wilhelm M, FrenzelA, HenrikssonM. The MYCN oncogene and differentiation in neuroblastoma. Seminars cancer Biol. 2011;21(4):256-266.

[27]

GuglielmiL, Cinnella C, NardellaM, et al. MYCN gene expression is required for the onset of the differentiation programme in neuroblastoma cells. Cell death & Dis. 2014;5(2):e1081.

[28]

HuangS, GongN, LiJ, et al. The role of ncRNAs in neuroblastoma: mechanisms, biomarkers and therapeutic targets. Biomark Res. 2022;10(1):18.

[29]

VeeraraghavanV, Jayaraman S, RengasamyG, et al. Deciphering the role of MicroRNAs in neuroblastoma. Molecules. 2021;27(1):99.

[30]

JauhariA, SinghT, PandeyA, et al. Differentiation induces dramatic changes in miRNA profile, where loss of dicer diverts differentiating SH-SY5Y cells toward senescence. Mol Neurobiol. 2017;54(7):4986-4995.

[31]

YeM, LiuB, ZhangJ, Dong K. Role of long noncoding RNA in neuroblastoma. Discov Med. 2020;30(160):71-82.

[32]

PandeyG, MitraS, SubhashS, et al. The risk-associated long noncoding RNA NBAT-1 controls neuroblastoma progression by regulating cell proliferation and neuronal differentiation. Cancer Cell. 2014;26(5):722-737.

[33]

Karami FathM, Pourbagher Benam S, SalmaniK, et al. Circular RNAs in neuroblastoma: pathogenesis, potential biomarker, and therapeutic target. Pathology, Res Pract. 2022;238:154094.

[34]

BrodeurG, Bagatell R. Mechanisms of neuroblastoma regression. Nat Rev Clin Oncol. 2014;11(12):704-713.

[35]

WuP, ChuangP, ChangG, et al. Novel endogenous ligands of aryl hydrocarbon receptor mediate neural development and differentiation of neuroblastoma. ACS Chem Neurosci. 2019;10(9):4031-4042.

[36]

FrummS, FanZ, RossK, et al. Selective HDAC1/HDAC2 inhibitors induce neuroblastoma differentiation. Chem Biol. 2013;20(5):713-725.

[37]

LiZ, Takenobu H, SetyawatiA, et al. EZH2 regulates neuroblastoma cell differentiation via NTRK1 promoter epigenetic modifications. Oncogene. 2018;37(20):2714-2727.

[38]

BayevaN, CollE, PiskarevaO. Differentiating neuroblastoma: a systematic review of the retinoic acid, its derivatives, and synergistic interactions. J Personalized Med. 2021;11(3):211.

[39]

StallingsR, FoleyN, BrayI, Das S, BuckleyP. MicroRNA and DNA methylation alterations mediating retinoic acid induced neuroblastoma cell differentiation. Seminars cancer Biol. 2011;21(4):283-290.

[40]

ChlapekP, Slavikova V, MazanekP, SterbaJ, Veselska R. Why differentiation therapy sometimes fails: molecular mechanisms of resistance to retinoids. Int J Mol Sci. 2018;19(1):132.

[41]

CheungW, ChuP, KwongY. Effects of arsenic trioxide on the cellular proliferation, apoptosis and differentiation of human neuroblastoma cells. Cancer Lett. 2007;246(1-2):122-128.

[42]

LiC, FengC, ChenY, et al. Arsenic trioxide induces the differentiation of retinoic acid-resistant neuroblastoma cells via upregulation of HoxC9. Adv Clin Exp Med official organ Wroclaw Med Univ. 2022;31(8):903-911.

[43]

BachL. IGF-binding proteins. J Mol Endocrinol. 2018;61(1):T11-T28.

[44]

LeRoithD, HollyJ, ForbesB. Insulin-like growth factors: ligands, binding proteins, and receptors. Mol Metabol. 2021;52:101245.

[45]

BaxterR. IGF binding proteins in cancer: mechanistic and clinical insights. Nat Rev Cancer. 2014;14(5):329-341.

[46]

JonesJI, Gockerman A, BusbyWH, Jr, Camacho-HubnerC, Clemmons DR. Extracellular matrix contains insulin-like growth factor binding protein-5: potentiation of the effects of IGF-I. J Cell Biol. 1993;121(3):679-687.

[47]

HamonGA, HuntTK, SpencerEM. In vivo effects of systemic insulin-like growth factor-I alone and complexed with insulin-like growth factor binding protein-3 on corticosteroid suppressed wounds. Growth Regul. 1993;3(1):53-56.

[48]

LeRoithD, HollyJMP, ForbesBE. Insulin-like growth factors: ligands, binding proteins, and receptors. Mol Metabol. 2021;52:101245.

[49]

LiuY, ShenS, YanZ, et al. Expression characteristics and their functional role of IGFBP gene family in pan-cancer. BMC Cancer. 2023;23(1):371.

[50]

ThomasD, Radhakrishnan P. Role of tumor and stroma-derived IGF/IGFBPs in pancreatic cancer. Cancers. 2020;12(5):1228.

[51]

KashyapM. Role of insulin-like growth factor-binding proteins in the pathophysiology and tumorigenesis of gastroesophageal cancers. Tumour biol J Int Soc Oncodevelopmental Biol Med. 2015;36(11):8247-8257.

[52]

PerksC, HollyJ. IGF binding proteins (IGFBPs) and regulation of breast cancer biology. J Mammary Gland Biol Neoplasia. 2008;13(4):455-469.

[53]

RussoV, Schütt B, AndaloroE, et al. Insulin-like growth factor binding protein-2 binding to extracellular matrix plays a critical role in neuroblastoma cell proliferation, migration, and invasion. Endocrinology. 2005;146(10):4445-4455.

[54]

AzarW, AzarS, HigginsS, et al. IGFBP-2 enhances VEGF gene promoter activity and consequent promotion of angiogenesis by neuroblastoma cells. Endocrinology. 2011;152(9):3332-3342.

[55]

JeongE, KimS, JungS, et al. Enhancement of IGF-2-induced neurite outgrowth by IGF-binding protein-2 and osteoglycin in SH-SY5Y human neuroblastoma cells. Neurosci Lett. 2013;548:249-254.

[56]

AzarW, Zivkovic S, WertherG, RussoV. IGFBP-2 nuclear translocation is mediated by a functional NLS sequence and is essential for its pro-tumorigenic actions in cancer cells. Oncogene. 2014;33(5):578-588.

[57]

ZhangD, Babayan L, HoH, HeaneyA. Chromogranin A regulates neuroblastoma proliferation and phenotype. Biol Open. 2019;8(3):bio036566.

[58]

TannoB, VitaliR, De ArcangelisD, et al. Bim-dependent apoptosis follows IGFBP-5 down-regulation in neuroblastoma cells. Biochem Biophys Res Commun. 2006;351(2):547-552.

[59]

CesiV, Giuffrida M, VitaliR, et al. C/EBP alpha and beta mimic retinoic acid activation of IGFBP-5 in neuroblastoma cells by a mechanism independent from binding to their site. Exp Cell Res. 2005;305(1):179-189.

[60]

TannoB, Negroni A, VitaliR, et al. Expression of insulin-like growth factor-binding protein 5 in neuroblastoma cells is regulated at the transcriptional level by c-Myb and B-Myb via direct and indirect mechanisms. J Biol Chem. 2002;277(26):23172-23180.

[61]

CesiV, VitaliR, TannoB, et al. Insulin-like growth factor binding protein 5: contribution to growth and differentiation of neuroblastoma cells. Ann N Y Acad Sci. 2004;1028:59-68.

[62]

BabajkoS, Leneuve P, LoretC, BinouxM. IGF-binding protein-6 is involved in growth inhibition in SH-SY5Y human neuroblastoma cells: its production is both IGF-and cell density-dependent. J Endocrinol. 1997;152(2):221-227.

[63]

SeurinD, Lassarre C, BienvenuG, BabajkoS. Insulin-like growth factor binding protein-6 inhibits neuroblastoma cell proliferation and tumour development. Eur J Cancer. 2002;38(15):2058-2065.

[64]

WeiL, WengX, HuangX, Peng Y, GuoH, XuY. IGFBP2 in cancer: pathological role and clinical significance (Review). Oncol Rep. 2021;45(2):427-438.

[65]

LonghitanoL, Vicario N, ForteS, et al. Lactate modulates microglia polarization via IGFBP6 expression and remodels tumor microenvironment in glioblastoma. Cancer Immunol Immunother. 2023;72(1):1-20.

[66]

LonghitanoL, ForteS, OrlandoL, et al. The crosstalk between GPR81/IGFBP6 promotes breast cancer progression by modulating lactate metabolism and oxidative stress. Antioxidants. 2022;11(2):275.

[67]

ZhaoC, ZhuX, WangG, Wang W, JuS, WangX. Decreased expression of IGFBP6 correlates with poor survival in colorectal cancer patients. Pathol, Res Pract. 2020;216(5):152909.

[68]

BachL, FuP, YangZ. Insulin-like growth factor-binding protein-6 and cancer. Clin Sci. 2013;124(4):215-229.

[69]

GrellierP, De Galle B, BabajkoS. Expression of insulin-like growth factor-binding protein 6 complementary DNA alters neuroblastoma cell growth. Cancer Res. 1998;58(8):1670-1676.

[70]

HanN, ZhangF, LiG, et al. Local application of IGFBP5 protein enhanced periodontal tissue regeneration via increasing the migration, cell proliferation and osteo/dentinogenic differentiation of mesenchymal stem cells in an inflammatory niche. Stem Cell Res & Ther. 2017;8(1):210.

[71]

TannoB, CesiV, VitaliR, et al. Silencing of endogenous IGFBP-5 by micro RNA interference affects proliferation, apoptosis and differentiation of neuroblastoma cells. Cell Death Differ. 2005;12(3):213-223.

[72]

LiuQ, WangZ, JiangY, et al. Single-cell landscape analysis reveals distinct regression trajectories and novel prognostic biomarkers in primary neuroblastoma. Gene & Dis. 2022;9(6):1624-1638.

[73]

KildisiuteG, Kholosy W, YoungM, et al. Tumor to normal single-cell mRNA comparisons reveal a pan-neuroblastoma cancer cell. Sci Adv. 2021;7(6).

[74]

JanskyS, SharmaA, KörberV, et al. Single-cell transcriptomic analyses provide insights into the developmental origins of neuroblastoma. Nat Genet. 2021;53(5):683-693.

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2024 The Authors. Pediatric Discovery published by John Wiley & Sons Australia, Ltd on behalf of Children’s Hospital of Chongqing Medical University.

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