Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

The Tumor Microenvironment02:17

The Tumor Microenvironment

8.0K
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...
8.0K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

5.0K
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...
5.0K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

7.3K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.3K
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

6.2K
Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
6.2K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

8.3K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.3K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

2.9K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Aneuploidy selects for the acquisition of driver genes in breast cancer.

Nature·2026
Same author

Hypoxia shapes both therapeutic response and resistance in metastatic clear cell renal cell carcinoma.

Cancer cell·2026
Same author

Multi-view deep learning of highly multiplexed imaging data improves association of cell states with clinical outcomes.

Bioinformatics advances·2026
Same author

Decoding TNBC architecture.

Nature cancer·2026
Same author

Pan-cancer N-glycoproteomic atlas of patient-derived xenografts uncovers FAT2 as an actionable surface target.

Cell reports. Medicine·2026
Same author

Medium-Chain Fatty Acid exposure in non-transformed mammary glands leads to pro-tumorigenic alterations associated with aging.

bioRxiv : the preprint server for biology·2025

Related Experiment Video

Updated: Mar 10, 2026

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
08:02

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells

Published on: September 23, 2021

3.1K

TIMPs: versatile extracellular regulators in cancer.

Hartland W Jackson1,2, Virginie Defamie1, Paul Waterhouse1

  • 1Department of Medical Biophysics, University of Toronto, Princess Margaret Cancer Centre, TMDT 301-13, 101 College Street, Toronto, Ontario, M5G IL7 Canada.

Nature Reviews. Cancer
|December 10, 2016
PubMed
Summary
This summary is machine-generated.

Tissue inhibitors of metalloproteinases (TIMPs) are key regulators in cancer development. Deregulation of TIMPs, particularly TIMP1 and TIMP3, impacts tumor progression and patient outcomes, offering potential therapeutic targets.

More Related Videos

LINE-1 Methylation Analysis in Mesenchymal Stem Cells Treated with Osteosarcoma-Derived Extracellular Vesicles
12:18

LINE-1 Methylation Analysis in Mesenchymal Stem Cells Treated with Osteosarcoma-Derived Extracellular Vesicles

Published on: February 1, 2020

6.2K
A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
09:52

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication

Published on: September 20, 2016

11.0K

Related Experiment Videos

Last Updated: Mar 10, 2026

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
08:02

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells

Published on: September 23, 2021

3.1K
LINE-1 Methylation Analysis in Mesenchymal Stem Cells Treated with Osteosarcoma-Derived Extracellular Vesicles
12:18

LINE-1 Methylation Analysis in Mesenchymal Stem Cells Treated with Osteosarcoma-Derived Extracellular Vesicles

Published on: February 1, 2020

6.2K
A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
09:52

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication

Published on: September 20, 2016

11.0K

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cancer biology aims to identify key tumorigenesis regulators for novel interventions.
  • Tissue inhibitors of metalloproteinases (TIMPs) are crucial regulators of pericellular proteolysis.
  • TIMPs influence tumor architecture and cell signaling pathways.

Purpose of the Study:

  • To review the role of the four non-redundant TIMPs in cancer.
  • To highlight the association of TIMP deregulation with cancer progression and prognosis.
  • To discuss future research directions for targeting TIMPs in cancer therapy.

Main Methods:

  • Review of experimental studies on TIMP function in cancer.
  • Analysis of TIMP deregulation in human cancers (tumor and stroma).
  • Correlation of specific TIMP alterations (TIMP1 overexpression, TIMP3 silencing) with cancer outcomes.

Main Results:

  • TIMPs contribute to multiple cancer hallmarks.
  • TIMP deregulation is a common feature in human cancers.
  • TIMP1 overexpression and TIMP3 silencing correlate with cancer progression and poor prognosis.

Conclusions:

  • TIMPs are critical players in tumorigenesis, affecting tumor architecture and signaling.
  • Specific TIMP alterations serve as prognostic biomarkers.
  • Future research should focus on protease-independent TIMP functions and therapeutic targeting.