Journal
MOLECULAR CANCER RESEARCH
Volume 17, Issue 8, Pages 1597-1604Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1541-7786.MCR-19-0286
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- Departments of Pediatrics and Genetics, Louisiana State University Health Sciences Center
- Children's Hospital (New Orleans, LA)
- NCI of the NIH [CA218764]
- LSU Research Enhancement Program
- LSU Leveraging Innovation for Technology Transfer (LIFT2) [HSCNO-2017-LIFT-008]
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [ZIADE000423] Funding Source: NIH RePORTER
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Insulinoma-associated-1 (IA-1 or INSM1) encodes a zincfinger transcription factor, which was isolated from a human insulinoma subtraction library, with specific expression patterns, predominantly in developing neuroendocrine tissues and tumors. INSM1 is key in early pancreatic endocrine, sympatho-adrenal lineage, and pan-neurogenic precursor development. Insm1 gene ablation results in impairment of pancreatic beta cells, catecholamine biosynthesis, and basal progenitor development during mammalian neocortex maturation. Recently, INSM1 has emerged as a superior, sensitive, and specific biomarker for neuroendocrine tumors. INSM1 regulates downstream target genes and exhibits extranuclear activities associated with multiple signaling pathways, including Sonic Hedgehog, PI3K/AKT, MEK/ERK1/2, ADK, p53, Wnt, histone acetylation, LSD1, cyclin D1, Ascl1, and N-myc. Novel strategies targeting INSM1-associated signaling pathways facilitate the suppression of neuroendocrine tumor growth. In addition, INSM1 promoter-driven reporter assay and/or suicide gene therapy are promising effective therapeutic approaches for targeted specific neuroendocrine tumor therapy. In this review, the current knowledge of the biological role of INSM1 as a neuroendocrine tumor biomarker is summarized, and novel strategies targeting multiple signaling pathways in the context of INSM1 expression in neuroendocrine tumors are further explored.
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