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Published on: August 23, 2019
IGFBP7: an oncosuppressor gene in thyroid carcinogenesis
M G Vizioli1, M Sensi, C Miranda
1Molecular Mechanisms Unit, Department of Experimental Oncology and Molecular Medicine, IRCCS Foundation--Istituto Nazionale dei Tumori, Milan, Italy.
Abstract:
Insulin-like growth factor-binding protein 7 (IGFBP7) is a secreted protein involved in several cellular processes, including proliferation, senescence and apoptosis. Loss of IGFBP7 expression is a critical step in the development of human tumors, including melanoma and colon cancer. By microarray gene expression studies, we have detected downregulation of IGFBP7 gene expression in follicular and papillary thyroid tumors in comparison with normal thyroid tissue. Evaluation of publicly available PTC microarray gene expression data sets confirmed, in a consistent fraction of tumors, the downregulation of IGFBP7 transcript levels. The functional consequence of IGFBP7 downregulation was addressed in the PTC-derived NIM1 cell line in which IGFBP7 expression is repressed by promoter hypermethylation. Exposure to soluble IGFBP7 protein or restoration of IGFBP7 expression by complementary DNA transfection reduced growth rate, migration, anchorage-independent growth and tumorigenicity of NIM1 cells. We show that the effects of IGFBP7 are related to apoptosis. Our data suggest that loss of IGFBP7 expression has a functional role in thyroid carcinogenesis, and it may represent a possible basis for therapeutic strategies.
Insights
Loss of Insulin-like growth factor-binding protein 7 (IGFBP7) expression is linked to thyroid cancer development. Restoring IGFBP7 levels inhibits tumor growth and migration, suggesting therapeutic potential.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Insulin-like growth factor-binding protein 7 (IGFBP7) is a secreted protein regulating cell proliferation, senescence, and apoptosis.
- Loss of IGFBP7 expression is implicated in various human cancers, including melanoma and colon cancer.
- Thyroid tumors exhibit altered gene expression patterns, necessitating investigation into specific molecular players.
Purpose of the Study:
- To investigate the role of IGFBP7 in thyroid carcinogenesis.
- To determine if IGFBP7 downregulation is a feature of thyroid tumors.
- To explore the functional consequences of IGFBP7 loss in thyroid cancer cells.
Main Methods:
- Microarray gene expression analysis of thyroid tumors and normal tissue.
- Bioinformatic evaluation of publicly available thyroid papillary cancer (PTC) datasets.
- Functional studies using the PTC-derived NIM1 cell line with repressed IGFBP7 expression.
- Assessment of cell proliferation, migration, anchorage-independent growth, and tumorigenicity.
- Investigation of apoptosis induction by IGFBP7.
Main Results:
- IGFBP7 gene expression was found to be downregulated in follicular and papillary thyroid tumors compared to normal thyroid tissue.
- Publicly available datasets confirmed consistent downregulation of IGFBP7 transcript levels in a fraction of PTCs.
- In the NIM1 cell line, repressed IGFBP7 expression due to promoter hypermethylation was observed.
- Reintroducing IGFBP7 protein or expression reduced cell growth rate, migration, anchorage-independent growth, and tumorigenicity.
- The anti-tumor effects of IGFBP7 were linked to the induction of apoptosis.
Conclusions:
- Loss of IGFBP7 expression plays a functional role in thyroid carcinogenesis.
- IGFBP7 downregulation is a significant event in thyroid tumor development.
- Restoration of IGFBP7 function presents a potential therapeutic strategy for thyroid cancer.
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