Single-cell RNA sequencing unveils tumor heterogeneity and immune microenvironment between subungual and plantar melanoma.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
25 Mar 2024
Historique:
received: 12 12 2023
accepted: 20 03 2024
medline: 26 3 2024
pubmed: 26 3 2024
entrez: 26 3 2024
Statut: epublish

Résumé

Acral melanoma (AM) is a subtype of melanoma with high prevalence in East Asians. AM is characterized by greater aggressiveness and lower survival rates. However, there are still fewer studies on immune mechanisms of AM especially subungual melanoma (SM) versus non-subungual melanoma (NSM). In order to explore tumor heterogeneity and immune microenvironment in different subtypes of AM, we applied single-cell RNA sequencing to 24,789 single cells isolated from the SM and plantar melanoma (PM) patients. Aspects of tumor heterogeneity, melanocytes from PM and SM had significant differences in gene expression, CNV and pathways in which tumor-associated such as NF-kb and Wnt were involved. Regarding the immune microenvironment, PM contained more fibroblasts and T/NK cells. The EPHA3-EFNA1 axis was expressed only in cancer-associated fibroblast (CAF) and melanocytes of PM, and the TIGIT-NECTIN2 axis was expressed in both AM subtypes of T/NK cells and melanocytes. Altogether, our study helps to elucidate the tumor heterogeneity in AM subpopulations and provides potential therapeutic targets for clinical research.

Identifiants

pubmed: 38528036
doi: 10.1038/s41598-024-57640-8
pii: 10.1038/s41598-024-57640-8
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

7039

Subventions

Organisme : Medical and Health Science and Technology Planning Project of Zhejiang Province
ID : 2021455749
Organisme : Zhejiang Natural Science Foundation of China
ID : LBZ22H160001
Organisme : Health Science and Technology Projects of Hangzhou
ID : A20220441

Informations de copyright

© 2024. The Author(s).

Références

Augustin, R. C. et al. Identification of tumor-intrinsic drivers of immune exclusion in acral melanoma. J. Immunother. Cancer https://doi.org/10.1136/jitc-2023-007567 (2023).
doi: 10.1136/jitc-2023-007567 pubmed: 37857525 pmcid: 10603348
Si, L. et al. Prevalence of BRAF V600E mutation in Chinese melanoma patients: Large scale analysis of BRAF and NRAS mutations in a 432-case cohort. Eur. J. Cancer https://doi.org/10.1016/j.ejca.2011.06.056 (2012).
doi: 10.1016/j.ejca.2011.06.056 pubmed: 21788131
Mao, L. et al. Palbociclib in advanced acral melanoma with genetic aberrations in the cyclin-dependent kinase 4 pathway. Eur. J. Cancer 148, 297–306. https://doi.org/10.1016/j.ejca.2021.02.021 (2021).
doi: 10.1016/j.ejca.2021.02.021 pubmed: 33770575
Hodi, F. S. et al. Imatinib for melanomas harboring mutationally activated or amplified KIT arising on mucosal, acral, and chronically sun-damaged skin. J. Clin. Oncol. 31, 3182–3190. https://doi.org/10.1200/JCO.2012.47.7836 (2013).
doi: 10.1200/JCO.2012.47.7836 pubmed: 23775962 pmcid: 4878082
Nakamura, Y. et al. Anti-PD1 checkpoint inhibitor therapy in acral melanoma: A multicenter study of 193 Japanese patients. Ann. Oncol. 31, 1198–1206. https://doi.org/10.1016/j.annonc.2020.05.031 (2020).
doi: 10.1016/j.annonc.2020.05.031 pubmed: 32522691
Guo, J. et al. Empowering therapeutic antibodies with IFN-α for cancer immunotherapy. PLoS ONE 14, e0219829. https://doi.org/10.1371/journal.pone.0219829 (2019).
doi: 10.1371/journal.pone.0219829 pubmed: 31393905 pmcid: 6687177
Newell, F. et al. Whole-genome sequencing of acral melanoma reveals genomic complexity and diversity. Nat. Commun. 11, 5259. https://doi.org/10.1038/s41467-020-18988-3 (2020).
doi: 10.1038/s41467-020-18988-3 pubmed: 33067454 pmcid: 7567804
Holman, B. N. et al. Clinical and molecular features of subungual melanomas are site-specific and distinct from acral melanomas. Melanoma Res. 30, 562–573. https://doi.org/10.1097/CMR.0000000000000688 (2020).
doi: 10.1097/CMR.0000000000000688 pubmed: 33156595
Whiteside, T. L. The tumor microenvironment and its role in promoting tumor growth. Oncogene 27, 5904–5912. https://doi.org/10.1038/onc.2008.271 (2008).
doi: 10.1038/onc.2008.271 pubmed: 18836471 pmcid: 3689267
Schoepp, M., Ströse, A. J. & Haier, J. Dysregulation of miRNA expression in cancer associated fibroblasts (CAFs) and its consequences on the tumor microenvironment. Cancers (Basel) https://doi.org/10.3390/cancers9060054 (2017).
doi: 10.3390/cancers9060054 pubmed: 28538690
Angell, H. & Galon, J. From the immune contexture to the Immunoscore: The role of prognostic and predictive immune markers in cancer. Curr. Opin. Immunol. 25, 261–267. https://doi.org/10.1016/j.coi.2013.03.004 (2013).
doi: 10.1016/j.coi.2013.03.004 pubmed: 23579076
Worboys, J. D. et al. TIGIT can inhibit T cell activation via ligation-induced nanoclusters, independent of CD226 co-stimulation. Nat. Commun. 14, 5016. https://doi.org/10.1038/s41467-023-40755-3 (2023).
doi: 10.1038/s41467-023-40755-3 pubmed: 37596248 pmcid: 10439114
Weulersse, M. et al. Eomes-dependent loss of the co-activating receptor CD226 restrains CD8+ T cell anti-tumor functions and limits the efficacy of cancer immunotherapy. Immunity 53, 824–839. https://doi.org/10.1016/j.immuni.2020.09.006 (2020).
doi: 10.1016/j.immuni.2020.09.006 pubmed: 33053331
Sheppard, K. E. & McArthur, G. A. The cell-cycle regulator CDK4: An emerging therapeutic target in melanoma. Clin. Cancer Res. 19, 5320–5328. https://doi.org/10.1158/1078-0432.CCR-13-0259 (2013).
doi: 10.1158/1078-0432.CCR-13-0259 pubmed: 24089445
Kong, Y. et al. Frequent genetic aberrations in the CDK4 Pathway in acral melanoma indicate the potential for CDK4/6 inhibitors in targeted therapy. Clin. Cancer Res. 23, 6946–6957. https://doi.org/10.1158/1078-0432.CCR-17-0070 (2017).
doi: 10.1158/1078-0432.CCR-17-0070 pubmed: 28830923
Rebecca, V. et al. ERK hyperactivation serves as a unified mechanism of escape in intrinsic and acquired CDK4/6 inhibitor resistance in acral lentiginous melanoma. Res. Sq. https://doi.org/10.21203/rs.3.rs-2817876/v1 (2023).
doi: 10.21203/rs.3.rs-2817876/v1 pubmed: 37131684 pmcid: 10153386
Van Hove, L. & Hoste, E. Activation of fibroblasts in skin cancer. J. Invest. Dermatol. 142, 1026–1031. https://doi.org/10.1016/j.jid.2021.09.010 (2022).
doi: 10.1016/j.jid.2021.09.010 pubmed: 34600919
Talia, M. et al. The Ephrin tyrosine kinase a3 (EphA3) is a novel mediator of RAGE-prompted motility of breast cancer cells. J. Exp. Clin. Cancer Res. 42, 164. https://doi.org/10.1186/s13046-023-02747-5 (2023).
doi: 10.1186/s13046-023-02747-5 pubmed: 37434266 pmcid: 10337103
Vail, M. E. et al. Inhibition of EphA3 expression in tumour stromal cells suppresses tumour growth and progression. Cancers (Basel) 15, 4646. https://doi.org/10.3390/cancers15184646 (2023).
doi: 10.3390/cancers15184646 pubmed: 37760615
Miao, H. et al. EphA2 promotes infiltrative invasion of glioma stem cells in vivo through cross-talk with Akt and regulates stem cell properties. Oncogene 34, 558–567. https://doi.org/10.1038/onc.2013.590 (2015).
doi: 10.1038/onc.2013.590 pubmed: 24488013
Nakamura, R. et al. EPHA2/EFNA1 expression in human gastric cancer. Cancer Sci. 96, 42–47 (2005).
doi: 10.1111/j.1349-7006.2005.00007.x pubmed: 15649254
Shi, Z.-Z. et al. Genomic profiling of rectal adenoma and carcinoma by array-based comparative genomic hybridization. BMC Med. Genom. 5, 52. https://doi.org/10.1186/1755-8794-5-52 (2012).
doi: 10.1186/1755-8794-5-52
Toma, M. I. et al. Lack of ephrin receptor A1 is a favorable independent prognostic factor in clear cell renal cell carcinoma. PLoS ONE 9, e102262. https://doi.org/10.1371/journal.pone.0102262 (2014).
doi: 10.1371/journal.pone.0102262 pubmed: 25025847 pmcid: 4099180
Miyazaki, K. et al. EphA4 is a prognostic factor in gastric cancer. BMC Clin. Pathol. 13, 19. https://doi.org/10.1186/1472-6890-13-19 (2013).
doi: 10.1186/1472-6890-13-19 pubmed: 23738943 pmcid: 3720259
Tang, W., Chen, J., Ji, T. & Cong, X. TIGIT, a novel immune checkpoint therapy for melanoma. Cell Death Dis. 14, 466. https://doi.org/10.1038/s41419-023-05961-3 (2023).
doi: 10.1038/s41419-023-05961-3 pubmed: 37495610 pmcid: 10372028
Xu, K. et al. Single-cell RNA sequencing reveals cell heterogeneity and transcriptome profile of breast cancer lymph node metastasis. Oncogenesis 10, 66. https://doi.org/10.1038/s41389-021-00355-6 (2021).
doi: 10.1038/s41389-021-00355-6 pubmed: 34611125 pmcid: 8492772
Takamatsu, K. et al. Profiling the inhibitory receptors LAG-3, TIM-3, and TIGIT in renal cell carcinoma reveals malignancy. Nat. Commun 12, 5547. https://doi.org/10.1038/s41467-021-25865-0 (2021).
doi: 10.1038/s41467-021-25865-0 pubmed: 34545095 pmcid: 8452744
Sun, Y. et al. Combined evaluation of the expression status of CD155 and TIGIT plays an important role in the prognosis of LUAD (lung adenocarcinoma). Int. Immunopharmacol. 80, 106198. https://doi.org/10.1016/j.intimp.2020.106198 (2020).
doi: 10.1016/j.intimp.2020.106198 pubmed: 31954274
Liu, X. et al. PD-1+ TIGIT+ CD8+ T cells are associated with pathogenesis and progression of patients with hepatitis B virus-related hepatocellular carcinoma. Cancer Immunol. Immunother. 68, 2041–2054. https://doi.org/10.1007/s00262-019-02426-5 (2019).
doi: 10.1007/s00262-019-02426-5 pubmed: 31720814
Ma, J. Bioinformatics-guided analysis uncovers TIGIT as an epigenetically regulated immunomodulator affecting immunotherapeutic sensitivity of gastric cancer. Cancer Biomark. 33, 349–358. https://doi.org/10.3233/CBM-210159 (2022).
doi: 10.3233/CBM-210159 pubmed: 34511485
Yang, Z.-Z. et al. TIGIT expression is associated with t-cell suppression and exhaustion and predicts clinical outcome and anti-PD-1 response in follicular lymphoma. Clin. Cancer Res. 26, 5217–5231. https://doi.org/10.1158/1078-0432.CCR-20-0558 (2020).
doi: 10.1158/1078-0432.CCR-20-0558 pubmed: 32631956
Shaffer, T., Natarajan, A. & Gambhir, S. S. PET imaging of TIGIT expression on tumor-infiltrating lymphocytes. Clin. Cancer Res. 27, 1932–1940. https://doi.org/10.1158/1078-0432.CCR-20-2725 (2021).
doi: 10.1158/1078-0432.CCR-20-2725 pubmed: 33408249
Zhang, J.-A. et al. Development of an immune-related gene signature for prognosis in melanoma. Front. Oncol. 10, 602555. https://doi.org/10.3389/fonc.2020.602555 (2020).
doi: 10.3389/fonc.2020.602555 pubmed: 33585219
Farrow, N. E. et al. Characterization of sentinel lymph node immune signatures and implications for risk stratification for adjuvant therapy in melanoma. Ann. Surg. Oncol. 28, 3501–3510. https://doi.org/10.1245/s10434-020-09277-w (2021).
doi: 10.1245/s10434-020-09277-w pubmed: 33205334
Inozume, T. et al. Melanoma cells control antimelanoma CTL responses via interaction between TIGIT and CD155 in the effector phase. J. Invest. Dermatol. 136, 255–263. https://doi.org/10.1038/JID.2015.404 (2016).
doi: 10.1038/JID.2015.404 pubmed: 26763445
Joller, N. et al. Cutting edge: TIGIT has T cell-intrinsic inhibitory functions. J. Immunol. 186, 1338–1342. https://doi.org/10.4049/jimmunol.1003081 (2011).
doi: 10.4049/jimmunol.1003081 pubmed: 21199897
Liu, S. et al. Recruitment of Grb2 and SHIP1 by the ITT-like motif of TIGIT suppresses granule polarization and cytotoxicity of NK cells. Cell Death Differ. 20, 456–464. https://doi.org/10.1038/cdd.2012.141 (2013).
doi: 10.1038/cdd.2012.141 pubmed: 23154388
Joller, N. et al. Treg cells expressing the coinhibitory molecule TIGIT selectively inhibit proinflammatory Th1 and Th17 cell responses. Immunity 40, 569–581. https://doi.org/10.1016/j.immuni.2014.02.012 (2014).
doi: 10.1016/j.immuni.2014.02.012 pubmed: 24745333 pmcid: 4070748
Fourcade, J. et al. CD226 opposes TIGIT to disrupt Tregs in melanoma. JCI Insight https://doi.org/10.1172/jci.insight.121157 (2018).
doi: 10.1172/jci.insight.121157 pubmed: 30046006 pmcid: 6124410
Lozano, E., Dominguez-Villar, M., Kuchroo, V. & Hafler, D. A. The TIGIT/CD226 axis regulates human T cell function. J. Immunol. 188, 3869–3875. https://doi.org/10.4049/jimmunol.1103627 (2012).
doi: 10.4049/jimmunol.1103627 pubmed: 22427644
Du, X. et al. CD226 regulates natural killer cell antitumor responses via phosphorylation-mediated inactivation of transcription factor FOXO1. Proc. Natl. Acad. Sci. U. S. A. 115, E11731–E11740. https://doi.org/10.1073/pnas.1814052115 (2018).
doi: 10.1073/pnas.1814052115 pubmed: 30504141 pmcid: 6294892
Rishiq, A., Bsoul, R., Pick, O. & Mandelboim, O. Studying TIGIT activity against tumors through the generation of knockout mice. Oncoimmunology 12, 2217735. https://doi.org/10.1080/2162402X.2023.2217735 (2023).
doi: 10.1080/2162402X.2023.2217735 pubmed: 37261087 pmcid: 10228407
Li, J. et al. Single-cell characterization of the cellular landscape of acral melanoma identifies novel targets for immunotherapy. Clin. Cancer Res. 28, 2131–2146. https://doi.org/10.1158/1078-0432.CCR-21-3145 (2022).
doi: 10.1158/1078-0432.CCR-21-3145 pubmed: 35247927 pmcid: 9106889

Auteurs

Panpan Wang (P)

Fourth Clinical College, Zhejiang Chinese Medical University, Hangzhou, China.

Yangyang Ma (Y)

Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, China.

Yige Zhao (Y)

Fourth Clinical College, Zhejiang Chinese Medical University, Hangzhou, China.

Yong Li (Y)

Research Center, Shanghai Yeslab Biotechnology, Shanghai, China.

Chenyu Tang (C)

Fourth Clinical College, Zhejiang Chinese Medical University, Hangzhou, China.

Shiwen Wang (S)

Fourth Clinical College, Zhejiang Chinese Medical University, Hangzhou, China.

Sha Jin (S)

Fourth Clinical College, Zhejiang Chinese Medical University, Hangzhou, China.

Jiaqi Wang (J)

Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, China.

Mengyan Zhu (M)

Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, China.

Bo Xie (B)

Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, China.

Ping Wang (P)

Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, China. dermwang@aliyun.com.

Classifications MeSH