Related Experiment Video
Updated: Feb 18, 2026

12:19
Three-Dimensional 3D Tumor Spheroid Invasion Assay
Published on: May 1, 2015
59.7K
Thrombospondin-1 is a multifaceted player in tumor progression
Tingting Huang1, Li Sun1, Xianglin Yuan1
1Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, PR China.
Oncotarget
|November 16, 2017
Summary
Thrombospondin-1 (TSP1), an extracellular matrix protein, plays a complex role in tumor microenvironments. Its effects on angiogenesis, tumor cell behavior, and immunity vary, impacting cancer progression.
Area of Science:
- Extracellular matrix biology
- Tumor microenvironment research
- Cancer immunology
Background:
- Thrombospondins are a family of extracellular matrix (ECM) proteins.
- Thrombospondin-1 (TSP1) is a key component of the tumor microenvironment.
- TSP1's functions are mediated by interactions with cell surface molecules.
Purpose of the Study:
- To review the multifaceted roles of TSP1 in tumor progression.
- To discuss TSP1's impact on angiogenesis, tumor cell behavior, and immunity.
- To explore the clinical implications of TSP1-related compounds.
Main Methods:
- Literature review of TSP1 functions in cancer.
- Analysis of TSP1's interactions with cellular and molecular components.
- Discussion of clinical studies involving TSP1.
Main Results:
- TSP1 acts as an angiogenesis inhibitor by affecting endothelial cells.
- TSP1 influences tumor cell adhesion, invasion, migration, proliferation, and apoptosis.
- TSP1 modulates tumor immunity.
- TSP1's effects are context-dependent, varying with the microenvironment.
Conclusions:
- TSP1 exhibits diverse and sometimes opposing effects on tumor progression.
- The composition of the tumor microenvironment dictates TSP1's impact.
- TSP1-based therapies hold potential clinical implications for cancer treatment.
Related Concept Videos
The Tumor Microenvironment
7.9K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
7.9K
Tumor Progression
7.5K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
7.5K
Metastasis
6.7K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
6.7K
Intracellular Signaling Affects Focal Adhesions
3.7K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Some...
3.7K
mTOR Signaling and Cancer Progression
4.9K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
4.9K
Cancer Cell Migration through Invadopodia
3.3K
Invadosome is a broad category of cell surface structures with proteolytic activity that degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
3.3K

