Int J Stomatol

Int J Stomatol ›› 2024, Vol. 51 ›› Issue (2): 208-216.doi: 10.7518/gjkq.2024027

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Role of advanced glycosylation end-products and their receptors in the progression and treatment of oral squamous cell carcinoma

Wenxuan Wang(),Yunkun Liu,Bingzhi Li,Nengwen Huang,Zeyu Hou,Jinru Tang,Longjiang Li()   

  1. State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & Dept. of Head and Neck Oncology, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2023-03-22 Revised:2023-08-18 Online:2024-03-01 Published:2024-03-11
  • Contact: Longjiang Li E-mail:wangwenxuan2533@163.com;muzili63@163.com
  • Supported by:
    National Natural Science Foundation of China(82141130)

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Abstract:

The molecular mechanisms underlying the occurrence and progression of oral squamous cell carcinoma (OSCC) are still not fully understood. This topic remains a focal point of research to comprehend the malignant biological characteristics of OSCC and explore targeted therapeutic approaches. Advanced glycation end-products (AGEs) and their receptors (RAGE) interact with other receptors in vivo, thereby activating multiple signaling pathways to induce the synthesis of interleukins, growth factors, and cytokine synthesis. Recent studies have shown that the activation of AGE/RAGE-related signaling pathways affects the proliferation, invasion, angiogenesis, and local recurrence of oral cancer and is associated with poor prognosis in patients with advanced oral cancer. This paper reviews the relationship between AGEs/RAGE and OSCC with the aim of providing potential targets for OSCC treatment.

Key words: oral squamous cell carcinoma, advanced glycation end-product, receptor of advanced glycation end-product

CLC Number: 

  • R739.8

TrendMD: 

Fig 1

The formation of AGE and its relationship with clinical diseases"

Fig 2

AGE‐RAGE axis signaling"

1 Ng JH, Iyer NG, Tan MH, et al. Changing epide-miology of oral squamous cell carcinoma of the tongue: a global study[J]. Head Neck, 2017, 39(2): 297-304.
2 Hu Y, Zhang XH, Ma YN, et al. Incident type 2 diabetes duration and cancer risk: a prospective study in two US cohorts[J]. J Natl Cancer Inst, 2021, 113(4): 381-389.
3 Wu CH, Wu TY, Li CC, et al. Impact of diabetes mellitus on the prognosis of patients with oral squamous cell carcinoma: a retrospective cohort study[J]. Ann Surg Oncol, 2010, 17(8): 2175-2183.
4 Yan LJ. Pathogenesis of chronic hyperglycemia: from reductive stress to oxidative stress[J]. J Diabetes Res, 2014, 2014: 137919.
5 Choudhuri S, Dutta D, Chowdhury IH, et al. Asso-ciation of hyperglycemia mediated increased advanced glycation and erythrocyte antioxidant enzyme activity in different stages of diabetic retinopathy[J]. Diabetes Res Clin Pract, 2013, 100(3): 376-384.
6 Sakamoto Y, Okui T, Yoneda T, et al. High-mobility group box 1 induces bone destruction associated with advanced oral squamous cancer via RAGE and TLR4[J]. Biochem Biophys Res Commun, 2020, 531(3): 422-430.
7 Ren LY, Lou Y, Sun MY. The anti-tumor effects of evodiamine on oral squamous cell carcinoma (OSCC) through regulating advanced glycation end products (AGE)/receptor for advanced glycation end products (RAGE) pathway[J]. Bioengineered, 2021, 12(1): 5985-5995.
8 Ko SY, Ko HA, Shieh TM, et al. Advanced glycation end products influence oral cancer cell survival via Bcl-xl and Nrf-2 regulation in vitro [J]. Oncol Lett, 2017, 13(5): 3328-3334.
9 Chapman S, Mick M, Hall P, et al. Cigarette smoke extract induces oral squamous cell carcinoma cell invasion in a receptor for advanced glycation end-products-dependent manner[J]. Eur J Oral Sci, 2018, 126(1): 33-40.
10 Ott C, Jacobs K, Haucke E, et al. Role of advanced glycation end products in cellular signaling[J]. Redox Biol, 2014, 2: 411-429.
11 Palanissami G, Paul SFD. RAGE and its ligands: molecular interplay between glycation, inflammation, and hallmarks of cancer-a review[J]. Horm Cancer, 2018, 9(5): 295-325.
12 Zhang WD, Randell EW, Sun G, et al. Hyperglycemia-related advanced glycation end-products is associated with the altered phosphatidylcholine meta-bolism in osteoarthritis patients with diabetes[J]. PLoS One, 2017, 12(9): e0184105.
13 Zeng C, Li YY, Ma JZ, et al. Clinical/translational aspects of advanced glycation end-products[J]. Trends Endocrinol Metab, 2019, 30(12): 959-973.
14 Rungratanawanich W, Qu Y, Wang X, et al. Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-media-ted tissue injury[J]. Exp Mol Med, 2021, 53(2): 168-188.
15 McRobert EA, Gallicchio M, Jerums G, et al. The amino-terminal domains of the ezrin, radixin, and moesin (ERM) proteins bind advanced glycation end products, an interaction that may play a role in the development of diabetic complications[J]. J Biol Chem, 2003, 278(28): 25783-25789.
16 Bierhaus A, Humpert PM, Morcos M, et al. Understanding RAGE, the receptor for advanced glycation end products[J]. J Mol Med Berlin Ger, 2005, 83(11): 876-886.
17 Oczypok EA, Perkins TN, Oury TD. All the “RAGE” in lung disease: the receptor for advanced glycation endproducts (RAGE) is a major mediator of pulmonary inflammatory responses[J]. Paediatr Respir Rev, 2017, 23: 40-49.
18 Teodorowicz M, Hendriks WH, Wichers HJ, et al. Immunomodulation by processed animal feed: the role of Maillard reaction products and advanced glycation end-products (AGEs)[J]. Front Immunol, 2018, 9: 2088.
19 Hudson BI, Lippman ME. Targeting RAGE signa-ling in inflammatory disease[J]. Annu Rev Med, 2018, 69: 349-364.
20 Leung SS, Forbes JM, Borg DJ. Receptor for advanced glycation end products (RAGE) in type 1 diabetes pathogenesis[J]. Curr Diab Rep, 2016, 16(10): 100.
21 Rojas A, Delgado-López F, González I, et al. The receptor for advanced glycation end-products: a complex signaling scenario for a promiscuous receptor[J]. Cell Signal, 2013, 25(3): 609-614.
22 Huang JS, Guh JY, Hung WC, et al. Role of the Janus kinase (JAK)/signal transducters and activators of transcription (STAT) cascade in advanced glycation end-product-induced cellular mitogenesis in NRK-49F cells[J]. Biochem J, 1999, 342(Pt 1): 231-238.
23 Mollace A, Coluccio ML, Donato G, et al. Cross-talks in colon cancer between RAGE/AGEs axis and inflammation/immunotherapy[J]. Oncotarget, 2021, 12(13): 1281-1295.
24 Gawlowski T, Stratmann B, Ruetter R, et al. Advanced glycation end products strongly activate platelets[J]. Eur J Nutr, 2009, 48(8): 475-481.
25 Sick E, Brehin S, André P, et al. Advanced glycation end products (AGEs) activate mast cells[J]. Br J Pharmacol, 2010, 161(2): 442-455.
26 Heidari F, Rabizadeh S, Mansournia MA, et al. Inflammatory, oxidative stress and anti-oxidative markers in patients with endometrial carcinoma and diabetes[J]. Cytokine, 2019, 120: 186-190.
27 Ashraf JM, Shahab U, Tabrez S, et al. DNA glycation from 3-deoxyglucosone leads to the formation of AGEs: potential role in cancer auto-antibodies[J]. Cell Biochem Biophys, 2016, 74(1): 67-77.
28 Chen M, Glenn JV, Dasari S, et al. RAGE regulates immune cell infiltration and angiogenesis in choroidal neovascularization[J]. PLoS One, 2014, 9(2): e89548.
29 Qian QQ, Zhang X, Wang YW, et al. Pro-inflammatory role of high-mobility group box-1 on brain mast cells via the RAGE/NF-κB pathway[J]. J Neurochem, 2019, 151(5): 595-607.
30 Nakamura N, Matsui T, Ishibashi Y, et al. RAGE-aptamer attenuates the growth and liver metastasis of malignant melanoma in nude mice[J]. Mol Med, 2017, 23: 295-306.
31 Ritter B, Greten FR. Modulating inflammation for cancer therapy[J]. J Exp Med, 2019, 216(6): 1234-1243.
32 Kolonin MG, Sergeeva A, Staquicini DI, et al. Interaction between tumor cell surface receptor RAGE and proteinase 3 mediates prostate cancer metastasis to bone[J]. Cancer Res, 2017, 77(12): 3144-3150.
33 Chen MC, Chen KC, Chang GC, et al. RAGE acts as an oncogenic role and promotes the metastasis of human lung cancer[J]. Cell Death Dis, 2020, 11(4): 265.
34 Kwak T, Drews-Elger K, Ergonul A, et al. Targeting of RAGE-ligand signaling impairs breast cancer cell invasion and metastasis[J]. Oncogene, 2017, 36(11): 1559-1572.
35 Ohgami N, Nagai R, Miyazaki A, et al. Scavenger receptor class B type Ⅰ -mediated reverse choleste-rol transport is inhibited by advanced glycation end products[J]. J Biol Chem, 2001, 276(16): 13348-13355.
36 Elangovan I, Thirugnanam S, Chen AS, et al. Targe-ting receptor for advanced glycation end products (RAGE) expression induces apoptosis and inhibits prostate tumor growth[J]. Biochem Biophys Res Commun, 2012, 417(4): 1133-1138.
37 Jandial R, Neman J, Lim PP, et al. Inhibition of GLO1 in glioblastoma multiforme increases DNA-AGEs, stimulates RAGE expression, and inhibits brain tumor growth in orthotopic mouse models[J]. Int J Mol Sci, 2018, 19(2): 406.
38 Chen XB, Zhang LY, Zhang IY, et al. RAGE expression in tumor-associated macrophages promotes angiogenesis in glioma[J]. Cancer Res, 2014, 74(24): 7285-7297.
39 Erusalimsky JD. The use of the soluble receptor for advanced glycation-end products (sRAGE) as a potential biomarker of disease risk and adverse outcomes[J]. Redox Biol, 2021, 42: 101958.
40 Tesarová P, Kalousová M, Jáchymová M, et al. Receptor for advanced glycation end products (RAGE): soluble form (sRAGE) and gene polymorphisms in patients with breast cancer[J]. Cancer Invest, 2007, 25(8): 720-725.
41 Jiao L, Weinstein SJ, Albanes D, et al. Evidence that serum levels of the soluble receptor for advanced glycation end products are inversely associated with pancreatic cancer risk: a prospective study[J]. Cancer Res, 2011, 71(10): 3582-3589.
42 Riuzzi F, Sorci G, Donato R. The amphoterin (HMGB1)/receptor for advanced glycation end products (RAGE) pair modulates myoblast proliferation, apoptosis, adhesiveness, migration, and invasiveness. Functional inactivation of RAGE in L6 myoblasts results in tumor formation in vivo [J]. J Biol Chem, 2006, 281(12): 8242-8253.
43 Blatt S, Krüger M, Ziebart T, et al. Biomarkers in diagnosis and therapy of oral squamous cell carcinoma: a review of the literature[J]. J Craniomaxillofac Surg, 2017, 45(5): 722-730.
44 Malik UU, Zarina S, Pennington SR. Oral squamous cell carcinoma: key clinical questions, biomarker discovery, and the role of proteomics[J]. Arch Oral Biol, 2016, 63: 53-65.
45 Nagaraj NS, Zacharias W. Cigarette smoke condensate increases cathepsin-mediated invasiveness of oral carcinoma cells[J]. Toxicol Lett, 2007, 170(2): 134-145.
46 Robinson AB, Johnson KD, Bennion BG, et al. RAGE signaling by alveolar macrophages influen-ces tobacco smoke-induced inflammation[J]. Am J Physiol Lung Cell Mol Physiol, 2012, 302(11): L1192-L1199.
47 Winden DR, Barton DB, Betteridge BC, et al. Antenatal exposure of maternal secondhand smoke (SHS) increases fetal lung expression of RAGE and induces RAGE-mediated pulmonary inflammation[J]. Respir Res, 2014, 15(1): 129.
48 Bhawal UK, Ozaki Y, Nishimura M, et al. Association of expression of receptor for advanced glycation end products and invasive activity of oral squamous cell carcinoma[J]. Oncology, 2005, 69(3): 246-255.
49 Lin CW, Chou YE, Yeh CM, et al. A functional va-riant at the miRNA binding site in HMGB1 gene is associated with risk of oral squamous cell carcinoma[J]. Oncotarget, 2017, 8(21): 34630-34642.
50 Supic G, Kozomara R, Zeljic K, et al. HMGB1 genetic polymorphisms in oral squamous cell carcinoma and oral lichen planus patients[J]. Oral Dis, 2015, 21(4): 536-543.
51 Su S, Chien M, Lin C, et al. RAGE gene polymorphism and environmental factor in the risk of oral cancer[J]. J Dent Res, 2015, 94(3): 403-411.
52 Ko SY, Ko HA, Shieh TM, et al. Cell migration is regulated by AGE-RAGE interaction in human oral cancer cells in vitro [J]. PLoS One, 2014, 9(10): e110542.
53 Okamoto T, Yamagishi S, Inagaki Y, et al. Angioge-nesis induced by advanced glycation end products and its prevention by cerivastatin[J]. FASEB J, 2002, 16(14): 1928-1930.
54 López-Graniel CM, Tamez de León D, Meneses-García A, et al. Tumor angiogenesis as a prognostic factor in oral cavity carcinomas[J]. J Exp Clin Cancer Res, 2001, 20(4): 463-468.
55 Schliephake H. Prognostic relevance of molecular markers of oral cancer: a review[J]. Int J Oral Maxillofac Surg, 2003, 32(3): 233-245.
56 Sasahira T, Kirita T, Bhawal UK, et al. The expression of receptor for advanced glycation end pro-ducts is associated with angiogenesis in human oral squamous cell carcinoma[J]. Virchows Arch, 2007, 450(3): 287-295.
57 Sasahira T, Kirita T, Bhawal UK, et al. Receptor for advanced glycation end products (RAGE) is important in the prediction of recurrence in human oral squamous cell carcinoma[J]. Histopathology, 2007, 51(2): 166-172.
58 Ahmad JG, Namin AW, Jorgensen JB, et al. Mandi-bular invasion by oral squamous cell carcinoma: clinicopathologic features of 74 cases[J]. Otolaryngol Head Neck Surg, 2019, 160(6): 1034-1041.
59 Shaw RJ, Brown JS, Woolgar JA, et al. The in-fluence of the pattern of mandibular invasion on recurrence and survival in oral squamous cell carcinoma[J]. Head Neck, 2004, 26(10): 861-869.
60 Dong XN, Qin A, Xu JK, et al. In situ accumulation of advanced glycation endproducts (AGEs) in bone matrix and its correlation with osteoclastic bone resorption[J]. Bone, 2011, 49(2): 174-183.
61 Kim H, Kim B, Kim SI, et al. S100A4 released from highly bone-metastatic breast cancer cells plays a critical role in osteolysis[J]. Bone Res, 2019, 7: 30.
62 Hwang ST, Um JY, Chinnathambi A, et al. Evodiamine mitigates cellular growth and promotes apoptosis by targeting the c-met pathway in prostate cancer cells[J]. Molecules, 2020, 25(6): 1320.
63 Kim SH, Kang JG, Kim CS, et al. Evodiamine suppresses survival, proliferation, migration and epithelial-mesenchymal transition of thyroid carcinoma cells[J]. Anticancer Res, 2018, 38(11): 6339-6352.
64 Zhao S, Xu K, Jiang R, et al. Evodiamine inhibits proliferation and promotes apoptosis of hepatocellular carcinoma cells via the Hippo-Yes-Associated Protein signaling pathway[J]. Life Sci, 2020, 251: 117424.
65 Sasahira T, Kirita T, Oue N, et al. High mobility group box-1-inducible melanoma inhibitory activity is associated with nodal metastasis and lymphangiogenesis in oral squamous cell carcinoma[J]. Cancer Sci, 2008, 99(9): 1806-1812.
66 Arcas A, Wilkinson DG, Nieto MÁ. The evolutio-nary history of ephs and ephrins: toward multicellular organisms[J]. Mol Biol Evol, 2020, 37(2): 379-394.
67 Chen YN, Zhang HM, Zhang YM. Targeting receptor tyrosine kinase EphB4 in cancer therapy[J]. Semin Cancer Biol, 2019, 56: 37-46.
68 Yi C, Zhang XL, Li HY, et al. EPHB4 regulates the proliferation and metastasis of oral squamous cell carcinoma through the HMGB1/NF‑κB signalling pathway[J]. J Cancer, 2021, 12(20): 5999-6011.
69 Tsujinaka H, Itaya-Hironaka A, Yamauchi A, et al. Statins decrease vascular epithelial growth factor expression via down-regulation of receptor for advanced glycation end-products[J]. Heliyon, 2017, 3(9): e00401.
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