About

Suzie Chen, PhD, is a Distinguished Professor Emeritus at Rutgers University, affiliated with the Ernest Mario School of Pharmacy. She holds a PhD and MS from the Albert Einstein College of Medicine and a BS from Trinity College. Her post-doctoral fellowship was completed at Columbia University. Dr. Chen's research focuses on the molecular mechanisms of melanoma development, utilizing transgenic mouse model systems, with particular involvement of the G-protein-coupled receptor Grm1 in controlling cell growth and differentiation. She has contributed significantly to the field through her involvement in various academic and research committees, including the Curriculum Committee, Strategic Steering Committee, and Dual Degree PharmD/MD Committee at Rutgers. Dr. Chen is also a member of the Rutgers Cancer Institute of New Jersey's Internal Advisory Board and has served on numerous NIH study sections and editorial boards for scientific journals. Her work has been recognized with awards such as the AAAS Fellow in 2016 for her contributions to translational research in melanoma biology, especially regarding glutamatergic signaling. She has been an invited speaker at international conferences and has received several honors for her research excellence.

Research topics

• Cancer research
• Biology
• Cell biology
• Immunology
• Chemistry
• Biotechnology
• Biochemistry
• Medicine

Selected publications

• Alpha-synuclein knockout impairs melanoma development and alters DNA damage repair in the TG3 mouse model in a sex-dependent manner

  Frontiers in Oncology · 2025-03-20 · 2 citations

  articleOpen access

  Introduction Strong evidence suggests links between Parkinson’s Disease (PD) and melanoma, as studies have found that people with PD are at an increased risk of developing melanoma and those with melanoma are at increased risk of developing PD. Although these clinical associations are well-established, the cellular and molecular pathways linking these diseases are poorly understood. Recent studies have found a previously unrecognized role for the neurodegeneration-associated protein alpha-synuclein (αSyn) in melanoma; the overexpression of αSyn promotes melanoma cell proliferation and metastasis. However, to our knowledge, no studies have investigated the role of αSyn in in vivo melanoma models outside of a xenograft paradigm. Methods Our study created and characterized Snca knockout in the spontaneously developing melanoma TG3 mouse line, TG3+/+ Snca -/-. Results We show that αSyn loss-of-function significantly delays melanoma onset and slows tumor growth in vivo in males. Furthermore, decreased tumor volume is correlated with a decreased DNA damage signature and increased apoptotic markers, indicating a role for αSyn in modulating the DNA damage response (DDR) pathway. Discussion Overall, our study may suggest that targeting αSyn and its role in modulating the DDR and melanomagenesis could serve as a promising new therapeutic target.

  PublisherOA PDFDOI

• In Vitro and In Vivo Studies of Melanoma Cell Migration by Antagonistic Mimetics of Adhesion Molecule L1CAM

  International Journal of Molecular Sciences · 2024-04-28 · 1 citations

  articleOpen accessSenior authorCorresponding

  Melanoma, the deadliest type of skin cancer, has a high propensity to metastasize to other organs, including the brain, lymph nodes, lungs, and bones. While progress has been made in managing melanoma with targeted and immune therapies, many patients do not benefit from these current treatment modalities. Tumor cell migration is the initial step for invasion and metastasis. A better understanding of the molecular mechanisms underlying metastasis is crucial for developing therapeutic strategies for metastatic diseases, including melanoma. The cell adhesion molecule L1CAM (CD171, in short L1) is upregulated in many human cancers, enhancing tumor cell migration. Earlier studies showed that the small-molecule antagonistic mimetics of L1 suppress glioblastoma cell migration in vitro. This study aims to evaluate if L1 mimetic antagonists can inhibit melanoma cell migration in vitro and in vivo. We showed that two antagonistic mimetics of L1, anagrelide and 2-hydroxy-5-fluoropyrimidine (2H5F), reduced melanoma cell migration in vitro. In in vivo allograft studies, only 2H5F-treated female mice showed a decrease in tumor volume.

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• An In Vivo Study of <scp>LNS8801</scp>, a <scp>GPER</scp> Agonist, in a Spontaneous Melanoma‐Prone Mouse Model, <scp>TGS</scp>

  Pigment Cell & Melanoma Research · 2024-09-16 · 2 citations

  articleOpen accessSenior author

  Melanoma is the most aggressive and deadly form of skin cancer that arises from the transformation of melanocytes, the pigment producing cells of the skin. In the year 2024 there will be approximately 10,000 new cases of melanoma diagnosed and approximately 8,000 deaths attributed to melanoma in the United States. In this study we treated a group of male and female transgenic mice that spontaneously develop metastatic melanoma, TGS, with a G-protein-coupled estrogen receptor agonist LNS8801 to assess the efficacy on disease progression. A second group of male and female TGS mice was also exposed to UVB irradiation to mimic exposure to sunlight. Over the course of the 32-week experiment, visible images were taken by the small animal imaging IVIS system to track tumor progression, and blood and tissue samples were collected for molecular analyses. Results showed that sex-biased effects were observed in the efficacy of LNS8801 and that LNS8801 shows a UV-protective influence in both male and female TGS mice.

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• Alpha-synuclein knockout impairs melanoma development and alters DNA damage repair in the TG3 mouse model in a sex-dependent manner

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-12-05 · 2 citations

  preprintOpen access

  ABSTRACT Strong evidence suggests links between Parkinson’s Disease (PD) and melanoma, as studies have found that people with PD are at an increased risk of developing melanoma and those with melanoma are at increased risk of developing PD. Although these clinical associations are well-established, the cellular and molecular pathways linking these diseases are poorly understood. Recent studies have found a previously unrecognized role for the neurodegeneration-associated protein alpha-synuclein (αSyn) in melanoma; the overexpression of αSyn promotes melanoma cell proliferation and metastasis. However, to our knowledge, no studies have investigated the role of αSyn in in vivo melanoma models outside of a xenograft paradigm. Our study created and characterized Snca knockout in the spontaneously developing melanoma TG3 mouse line, TG3+/+ Snca -/-. We show that αSyn loss-of-function significantly delays melanoma onset and slows tumor growth in vivo . Furthermore, decreased tumor volume is correlated with a decreased DNA damage signature and increased apoptotic markers, indicating a role for αSyn in modulating the DNA damage response (DDR) pathway. Overall, our study provides evidence that targeting αSyn and its role in modulating the DDR and melanomagenesis could serve as a promising new therapeutic target.

  PublisherOA PDFDOI

• U1 Adaptor Oligonucleotides Targeting BCL2 and GRM1 Suppress Growth of Human Melanoma Xenografts In Vivo

  Molecular Therapy — Nucleic Acids · 2024

  • Cancer research
  • Chemistry
  • Cell biology

  [This corrects the article DOI: 10.1038/mtna.2013.24.].

  PublisherDOI

• Current State of Melanoma Therapy and Next Steps: Battling Therapeutic Resistance

  Cancers · 2024-04-19 · 46 citations

  articleOpen accessSenior authorCorresponding

  Melanoma is the most aggressive and deadly form of skin cancer due to its high propensity to metastasize to distant organs. Significant progress has been made in the last few decades in melanoma therapeutics, most notably in targeted therapy and immunotherapy. These approaches have greatly improved treatment response outcomes; however, they remain limited in their abilities to hinder disease progression due, in part, to the onset of acquired resistance. In parallel, intrinsic resistance to therapy remains an issue to be resolved. In this review, we summarize currently available therapeutic options for melanoma treatment and focus on possible mechanisms that drive therapeutic resistance. A better understanding of therapy resistance will provide improved rational strategies to overcome these obstacles.

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• Assessing Longitudinal Treatment Efficacies and Alterations in Molecular Markers Associated with Glutamatergic Signaling and Immune Checkpoint Inhibitors in a Spontaneous Melanoma Mouse Model

  JID Innovations · 2024-01-19 · 1 citations

  articleOpen accessSenior authorCorresponding

  Previous work done by our laboratory described the use of an immunocompetent spontaneous melanoma-prone mouse model, TGS (TG-3/SKH-1), to evaluate treatment outcomes using inhibitors of glutamatergic signaling and immune checkpoint for 18 weeks. We showed a significant therapeutic efficacy with a notable sex-biased response in male mice. In this follow-up 18-week study, the dose of the glutamatergic signaling inhibitor was increased (from 1.7 mg/kg to 25 mg/kg), which resulted in improved responses in female mice but not male mice. The greatest reduction in tumor progression was observed in male mice treated with single-agent troriluzole and anti–PD-1. Furthermore, a randomly selected group of mice was removed from treatment after 18 weeks and maintained for up to an additional 48 weeks demonstrating the utility of the TGS mouse model to perform a ≥1-year preclinical therapeutic study in a physiologically relevant tumor–host environment. Digital spatial imaging analyses were performed in tumors and tumor microenvironments across treatment modalities using antibody panels for immune cell types and immune cell activation. The results suggest that immune cell populations and cytotoxic activities of T cells play critical roles in treatment responses in these mice. Examination of a group of molecular protein markers based on the proposed mechanisms of action of inhibitors of glutamatergic signaling and immune checkpoint showed that alterations in expression levels of xCT, γ-H2AX, EAAT2, PD-L1, and PD-1 are likely associated with the loss of treatment responses. These results suggest the importance of tracking changes in molecular markers associated with the mechanism of action of therapeutics over the course of a longitudinal preclinical therapeutic study in spatial and temporal manners. Previous work done by our laboratory described the use of an immunocompetent spontaneous melanoma-prone mouse model, TGS (TG-3/SKH-1), to evaluate treatment outcomes using inhibitors of glutamatergic signaling and immune checkpoint for 18 weeks. We showed a significant therapeutic efficacy with a notable sex-biased response in male mice. In this follow-up 18-week study, the dose of the glutamatergic signaling inhibitor was increased (from 1.7 mg/kg to 25 mg/kg), which resulted in improved responses in female mice but not male mice. The greatest reduction in tumor progression was observed in male mice treated with single-agent troriluzole and anti–PD-1. Furthermore, a randomly selected group of mice was removed from treatment after 18 weeks and maintained for up to an additional 48 weeks demonstrating the utility of the TGS mouse model to perform a ≥1-year preclinical therapeutic study in a physiologically relevant tumor–host environment. Digital spatial imaging analyses were performed in tumors and tumor microenvironments across treatment modalities using antibody panels for immune cell types and immune cell activation. The results suggest that immune cell populations and cytotoxic activities of T cells play critical roles in treatment responses in these mice. Examination of a group of molecular protein markers based on the proposed mechanisms of action of inhibitors of glutamatergic signaling and immune checkpoint showed that alterations in expression levels of xCT, γ-H2AX, EAAT2, PD-L1, and PD-1 are likely associated with the loss of treatment responses. These results suggest the importance of tracking changes in molecular markers associated with the mechanism of action of therapeutics over the course of a longitudinal preclinical therapeutic study in spatial and temporal manners.

  PublisherOA PDFDOI

• Study on the Complex Melanoma

  Cancers · 2024-02-20 · 1 citations

  editorialOpen accessSenior authorCorresponding

  Melanoma only accounts for about 1% of cases in skin cancer, unlike basal cell and/or squamous cell carcinomas; however, it owes its notoriety to being the deadliest type of skin cancer [...].

  PublisherOA PDFDOI

• Supplementary Table S1 from Riluzole Enhances Ionizing Radiation–Induced Cytotoxicity in Human Melanoma Cells that Ectopically Express Metabotropic Glutamate Receptor 1 &lt;i&gt;In Vitro&lt;/i&gt; and &lt;i&gt;In Vivo&lt;/i&gt;

  2023-03-31

  supplementary-materialsOpen access

  &lt;p&gt;Supplementary Table S1.&lt;/p&gt;

  PublisherDOI

• Supplementary Figure 1 from Activation of the Glutamate Receptor GRM1 Enhances Angiogenic Signaling to Drive Melanoma Progression

  2023-03-30

  preprintOpen access

  &lt;p&gt;PDF file - 737KB, Supplemental Figure 1: Apoptosis antibody array result of Uacc903-V1 and -G2.&lt;/p&gt;

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01CA074077

  NIH · $1.4M · 2004

• Translational application of mouse models of melanoma brain metastases

  NIH · 2017–2025

• NIH Grant R21CA185835

  NIH · $371k · 2017

• NIH Grant R01CA108720

  NIH · $1.3M · 2010

Frequent coauthors

• James S. Goydos

  129 shared

• B. Wall

  73 shared

• Seung‐Shick Shin

  68 shared

• Mirjana Efremova

  Queen Mary University of London

  45 shared

• Zlatko Trajanoski

  Innsbruck Medical University

  45 shared

• Christoph H. Tripp

  Innsbruck Medical University

  44 shared

• Patrizia Stoitzner

  Universität Innsbruck

  44 shared

• Giuseppe Cappellano

  Università degli Studi del Piemonte Orientale “Amedeo Avogadro”

  42 shared

Education

• Ph.D., Genetics

  Yeshiva University Albert Einstein College of Medicine

  1979

Awards & honors

• 2016 – AAAS Fellow, "For significant contributions in transl…
• 2016 – Invited Speaker at 4th GPCR in Drug Discovery
• 2007 – Second International Melanoma Congress Best Abstract…
• 2005 – Rutgers University Board of Trustees Award for Excell…
• 2005 – Keynote Speaker at Brain Tumor Center Seminar Series,…