Vascular endothelial growth factor/semaphorin-3A ratio and SEMA3A expression in cutaneous malignant melanoma.


Journal

Melanoma research
ISSN: 1473-5636
Titre abrégé: Melanoma Res
Pays: England
ID NLM: 9109623

Informations de publication

Date de publication:
10 2020
Historique:
pubmed: 10 6 2020
medline: 29 7 2021
entrez: 10 6 2020
Statut: ppublish

Résumé

Breslow thickness and Clark level are still important factors for cutaneous melanoma, but do not provide a precise prognosis in all cases. It is necessary to find new factors capable of a more accurate prediction of the tumor course. Angiogenesis is essential for tumor development and progression and is regulated by vascular endothelial growth factor A (VEGF-A) and semaphorins (SEMA), in particular, SEMA3A inhibits angiogenesis by affecting VEGF signaling. However, the prognostic role of angiogenetic factors remains unclear. To date, no information is available on SEMA3A in human melanoma. Microvessel density, immunohistochemical and mRNA VEGF and SEMA3A expression level in 60 thin (Breslow thickness ≤ 1.0 mm), 60 intermediate (1.1-4.0 mm) and 50 thick (>4.0 mm) primary human cutaneous melanomas were investigated and related to clinical/pathological parameters and disease-specific survival. No positive association between Breslow thickness, Clark level, metastasis presence and survival was identified; Clark level was poorly related to survival. VEGF and microvessel density were significantly higher in intermediate and thick melanomas and related to Breslow thickness and Clark level but not to metastasis status and survival. On the contrary, SEMA3A was significantly reduced in intermediate and thick melanomas and associated to metastasis and poor survival. VEGF/SEMA3A ratio was higher in the worst prognosis, resulting the most closely related factor with metastasis and survival. SEMA3A expression and VEGF/SEMA3A ratio turned out to be valuable prognostic biomarkers in patients affected by cutaneous melanoma, in particular with Breslow thickness >1 mm. SEMA3A might serve as a candidate tumor suppressor in cutaneous melanoma therapy.

Identifiants

pubmed: 32516239
doi: 10.1097/CMR.0000000000000674
pii: 00008390-202010000-00002
doi:

Substances chimiques

SEMA3A protein, human 0
Semaphorin-3A 0
VEGFA protein, human 0
Vascular Endothelial Growth Factor A 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

433-442

Références

Rastrelli M, Tropea S, Rossi CR, Alaibac M. Melanoma: epidemiology, risk factors, pathogenesis, diagnosis and classification. In Vivo. 2014; 28:1005–1011
Mimeault M, Batra SK. Novel biomarkers and therapeutic targets for optimizing the therapeutic management of melanomas. World J Clin Oncol. 2012; 3:32–42
Balch CM, Balch GC, Sharma RR. Identifying early melanomas at higher risk for metastases. J Clin Oncol. 2012; 30:1406–1407
Homsi J, Kashani-Sabet M, Messina JL, Daud A. Cutaneous melanoma: prognostic factors. Cancer Control. 2005; 12:223–229
Criscione VD, Weinstock MA. Melanoma thickness trends in the United States, 1988-2006. J Invest Dermatol. 2010; 130:793–797
Bartlett EK, Karakousis GC. Current staging and prognostic factors in melanoma. Surg Oncol Clin N Am. 2015; 24:215–227
Donovan P, Patel J, Dight J, Wong HY, Sim SL, Murigneux V, et al. Endovascular progenitors infiltrate melanomas and differentiate towards a variety of vascular beds promoting tumor metastasis. Nat Commun. 2019; 10:18
Zachary I. Signaling mechanisms mediating vascular protective actions of vascular endothelial growth factor. Am J Physiol Cell Physiol. 2001; 280:C1375–C1386
Simonetti O, Lucarini G, Brancorsini D, Nita P, Bernardini ML, Biagini G, Offidani A. Immunohistochemical expression of vascular endothelial growth factor, matrix metalloproteinase 2, and matrix metalloproteinase 9 in cutaneous melanocytic lesions. Cancer. 2002; 95:1963–1970
Alessi C, Scapulatempo Neto C, Viana CR, Vazquez VL. PD-1/PD-L1 and VEGF-A/VEGF-C expression in lymph node microenvironment and association with melanoma metastasis and survival. Melanoma Res. 2017; 27:565–572
Felcht M, Thomas M. Angiogenesis in malignant melanoma. J Dtsch Dermatol Ges. 2015; 13:125–136
Ronca M, Benkheil S, Mitola S, Struyf S, Liekens S. Tumor angiogenesis revisited: regulators and clinical implications. Med Res Rev. 2017; 37:1231–1274
Staton CA. Class 3 semaphorins and their receptors in physiological and pathological angiogenesis. Biochem Soc Trans. 2011; 39:1565–1570
Tamagnone L, Comoglio PM. Signalling by semaphorin receptors: cell guidance and beyond. Trends Cell Biol. 2000; 10:377–383
Chakraborty G, Kumar S, Mishra R, Patil TV, Kundu GC. Semaphorin 3A suppresses tumor growth and metastasis in mice melanoma model. PLoS One. 2012; 7:e33633
Simonetti O, Goteri G, Lucarini G, Filosa A, Pieramici T, Rubini C, et al. Potential role of CCL27 and CCR10 expression in melanoma progression and immune escape. Eur J Cancer. 2006; 42:1181–1187
Lever WF, Schaumburg-Lever G. Histopathology of the skin. 1990, Philadelphia, PA: J.B. Lippincott
Gupta GP, Massagué J. Cancer metastasis: building a framework. Cell. 2006; 127:679–695
Spatz A, Stock N, Batist G, van Kempen LC. The biology of melanoma prognostic factors. Discov Med. 2010; 10:87–93
White RR, Stanley WE, Johnson JL, Tyler DS, Seigler HF. Long-term survival in 2,505 patients with melanoma with regional lymph node metastasis. Ann Surg. 2002; 235:879–887
Pontikes LA, Temple WJ, Cassar SL, Lafrenière R, Huchcroft SA, Jerry LM, et al. Influence of level and depth on recurrence rate in thin melanomas. Am J Surg. 1993; 165:225–228
Martínez-García MÁ, Riveiro-Falkenbach E, Rodríguez-Peralto JL, Nagore E, Martorell-Calatayud A, Campos-Rodríguez F, et al.; Spanish Sleep Network. A prospective multicenter cohort study of cutaneous melanoma: clinical staging and potential associations with HIF-1α and VEGF expressions. Melanoma Res. 2017; 27:558–564
Chua R, Setzer S, Govindarajan B, Sexton D, Cohen C, Arbiser JL. Maspin expression, angiogenesis, prognostic parameters, and outcome in malignant melanoma. J Am Acad Dermatol. 2009; 60:758–766
Rajabi P, Neshat A, Mokhtari M, Rajabi MA, Eftekhari M, Tavakoli P. The role of VEGF in melanoma progression. J Res Med Sci. 2012; 17:534–539
Pastushenko I, Vermeulen PB, Carapeto FJ, Van den Eynden G, Rutten A, Ara M, et al. Blood microvessel density, lymphatic microvessel density and lymphatic invasion in predicting melanoma metastases: systematic review and meta-analysis. Br J Dermatol. 2014; 170:66–77
Ferrara N, Adamis AP. Ten years of anti-vascular endothelial growth factor therapy. Nat Rev Drug Discov. 2016; 15:385–403
Grignol VP, Olencki T, Relekar K, Taylor C, Kibler A, Kefauver C, et al. A phase 2 trial of bevacizumab and high-dose interferon alpha 2B in metastatic melanoma. J Immunother. 2011; 34:509–515
Varker KA, Biber JE, Kefauver C, Jensen R, Lehman A, Young D, et al. A randomized phase 2 trial of bevacizumab with or without daily low-dose interferon alfa-2b in metastatic malignant melanoma. Ann Surg Oncol. 2007; 14:2367–2376
Potente M, Gerhardt H, Carmeliet P. Basic and therapeutic aspects of angiogenesis. Cell. 2011; 146:873–887
Soker S, Takashima S, Miao HQ, Neufeld G, Klagsbrun M. Neuropilin-1 is expressed by endothelial and tumor cells as an isoform-specific receptor for vascular endothelial growth factor. Cell. 1998; 92:735–745
Bielenberg DR, Klagsbrun M. Targeting endothelial and tumor cells with semaphorins. Cancer Metastasis Rev. 2007; 26:421–431
Guttmann-Raviv N, Shraga-Heled N, Varshavsky A, Guimaraes-Sternberg C, Kessler O, Neufeld G. Semaphorin-3A and semaphorin-3F work together to repel endothelial cells and to inhibit their survival by induction of apoptosis. J Biol Chem. 2007; 282:26294–26305
Osada R, Horiuchi A, Kikuchi N, Ohira S, Ota M, Katsuyama Y, Konishi I. Expression of semaphorins, vascular endothelial growth factor, and their common receptor neuropilins and alleic loss of semaphorin locus in epithelial ovarian neoplasms: increased ratio of vascular endothelial growth factor to semaphorin is a poor prognostic factor in ovarian carcinomas. Hum Pathol. 2006; 37:1414–1425
Tang C, Gao X, Liu H, Jiang T, Zhai X. Decreased expression of SEMA3A is associated with poor prognosis in gastric carcinoma. Int J Clin Exp Pathol. 2014; 7:4782–4794
Herman JG, Meadows GG. Increased class 3 semaphorin expression modulates the invasive and adhesive properties of prostate cancer cells. Int J Oncol. 2007; 30:1231–1238
Kigel B, Varshavsky A, Kessler O, Neufeld G. Successful inhibition of tumor development by specific class-3 semaphorins is associated with expression of appropriate semaphorin receptors by tumor cells. PLoS One. 2008; 3:e3287
Bachelder RE, Lipscomb EA, Lin X, Wendt MA, Chadborn NH, Eickholt BJ, Mercurio AM. Competing autocrine pathways involving alternative neuropilin-1 ligands regulate chemotaxis of carcinoma cells. Cancer Res. 2003; 63:5230–5233
Bagnard D, Vaillant C, Khuth ST, Dufay N, Lohrum M, Puschel AW, et al. Semaphorin 3A-vascular endothelial growth factor-165 balance mediates migration and apoptosis of neural progenitor cells by the recruitment of shared receptor. J Neurosci. 2001; 21:3332–3341
Mazurek AM, Olbryt M. The influence of neuropilin-1 silencing on semaphorin 3A and 3C activity in B16(F10) murine melanoma cells. Neoplasma. 2012; 59:43–51
Maione F, Molla F, Meda C, Latini R, Zentilin L, Giacca M, et al. Semaphorin 3A is an endogenous angiogenesis inhibitor that blocks tumor growth and normalizes tumor vasculature in transgenic mouse models. J Clin Invest. 2009; 119:3356–3372
Gaur P, Bielenberg DR, Samuel S, Bose D, Zhou Y, Gray MJ, et al. Role of class 3 semaphorins and their receptors in tumor growth and angiogenesis. Clin Cancer Res. 2009; 15:6763–6770

Auteurs

Guendalina Lucarini (G)

Department of Clinic and Molecular Sciences, Histology.

Oriana Simonetti (O)

Dermatological Clinic.

Raffaella Lazzarini (R)

Department of Clinic and Molecular Sciences, Histology.

Federica Giantomassi (F)

Unit of Pathologic Anatomy and Histopathology, Polytechnic University of Marche Region, United Ancona Hospitals, Torrette, Ancona, Italy.

Gaia Goteri (G)

Unit of Pathologic Anatomy and Histopathology, Polytechnic University of Marche Region, United Ancona Hospitals, Torrette, Ancona, Italy.

Annamaria Offidani (A)

Dermatological Clinic.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH