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INTERNATIONAL CONGRESS OF

CancerGenetics

• The Role of S100B Protein in Promoting Metastasis in Small Cell Lung Cancer: Molecular Mechanisms and Therapeutic Implications – A Narrative Review

• Kourosh Amirian Shayesteh,^1,* Ahmadreza Sobhani,² Yalda Yousefnezhad,³
  1. Students Research Committee, Faculty of medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Iran
  2. Students Research Committee, Faculty of medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Iran
  3. Students Research Committee, Faculty of medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Iran
  
  
  
• Introduction: Small cell lung cancer (SCLC) is a well-established, highly malignant neuroendocrine tumor characterized by rapid proliferation, early dissemination, and dismal survival rates. Despite recent advancements in therapy management, metastasis continues to result in treatment failure and patient fatality. Recent findings suggest that S100B, a calcium-binding non-kinase member from the S100 protein family, may play an active role in the metastatic process. The S100B levels were elevated in patients with bone metastases, suggesting its potential as a serological biomarker for early detection and monitoring of tumor development. S100B enhances tumor invasiveness by its influence on many signaling pathways associated with tumorigenesis, apoptosis, and differentiation. The molecular pathways encompass processes regulating the p53 tumor suppressor pathway, the MAPK/ERK pathway, and the NF-κB activation pathway, all of which contribute to cancer progression. Additionally, S100B facilitates tumor cell survival and proliferation, as well as invasion and migration during the metastatic phase, predominantly to the brain. It also contributes to the formation of new blood vessels and regulates the immune system; the tumor acquires the ability to metastasis to other locations in the body. Due of S100B's role in tumor growth, there is growing interest in its potential as a therapeutic target. The primary ways to mitigate S100B activity have been delineated and encompass: the application of small molecule inhibitors, monoclonal antibodies, and RNA-based treatments. The proposed solutions aim to obstruct the binding of S100B to its downstream targets, hence reducing metastatic signaling and facilitating apoptotic processes. This review evaluates the molecular mechanisms by which S100B contributes to SCLC metastasis and its potential as a prognostic biomarker or therapeutic target to improve prognosis and survival.
• Methods: This study was conducted as a narrative review by systematically searching PubMed Scopus Web of Science data with relevant keywords. The research used the search terms S100B together with SCLC metastasis and tumor biomarkers and therapeutic targeting of S100B. The selection of studies happened through a relevance-based approach to understand SCLC progression and explore both diagnostic and therapeutic applications of S100B. The research study evaluates the diverse effects of S100B protein on cancer cell invasion in addition to tumor spread and new blood vessel formation and immunological system alterations. This review examined multiple potential therapeutic approaches that consisted of small molecule inhibitors and monoclonal antibodies together with RNA-based therapies for managing S100B-induced metastatic progression. The article examines forthcoming perspectives regarding using S100B-focused therapies within tailored SCLC treatment strategies.
• Results: Analysis of the literature indicates that substantial elevation of S100B in metastatic SCLC terminals especially in cases with bone metastases together with brain metastases. Research shows S100B hinders the tumor suppressor p53 and activates the MAPK/ERK pathway and advances NF-κB signaling which leads to tumor growth alongside invasion and apoptosis resistance. The process of angiogenesis and immune system avoidance becomes more prevalent due to S100B activity which boosts the metastatic potential of SCLC cells. Nonclinical research has demonstrated the potential effectiveness of S100B blocking agents through small molecule inhibitors and monoclonal antibodies to inhibit S100B activity and decrease metastatic disease development. The oncogenic effects of S100B protein can be reduced through RNA-based therapy approaches which utilize siRNA and antisense oligonucleotides.
• Conclusion: S100B plays a critical role in the metastatic progression of SCLC by modulating key oncogenic pathways, contribute to tumor cell survival, and facilitating invasion and angiogenesis. Given its strong relation with tumor aggressiveness and poor prognosis, S100B emerges as a promising prognostic biomarker for SCLC metastasis. Additionally, therapeutic strategies targeting S100B hold potential in disrupting metastatic signaling and enhancing the efficacy of existing treatments. Future clinical studies are warranted to further validate S100B as a therapeutic target and explore its potential integration into personalized treatment strategies for SCLC patients.
• Keywords: S100B protein, Small cell lung cancer (SCLC), Cancer Metastasis Biomarkers, Targeted therapy