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

Cancer02:18

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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,...
Metastasis02:30

Metastasis

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...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

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...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

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, invadopodia can...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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,...

You might also read

Related Articles

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

Sort by
Same author

Therapeutic zinc targets dysregulated GC-C signaling and restores ileal defects in a preclinical model of familial diarrheal disease.

American journal of physiology. Gastrointestinal and liver physiology·2026
Same author

Direct Printing of Electronics on Flexible Porous Substrates.

Small (Weinheim an der Bergstrasse, Germany)·2026
Same author

Glucose deprivation induces AMPK-dependent α-actinin-4 expression to sustain energy efficient non-proteolytic migration.

Journal of cell science·2026
Same author

Glycation-Driven Impairment of Cytoskeletal Homeostasis and Viability Disables Glyoxalase-Low Mesothelia From Resisting Cancer Colonization.

Journal of cellular physiology·2026
Same author

Prediction of Piconewton Receptor Tension Images using Deep Learning.

bioRxiv : the preprint server for biology·2026
Same author

Downregulation of Decorin in ovarian cancer cells and colonization microenvironment drives progression.

Biointerphases·2025

Related Experiment Video

Updated: Jun 25, 2026

Longitudinal Measurement of Extracellular Matrix Rigidity in 3D Tumor Models Using Particle-tracking Microrheology
11:11

Longitudinal Measurement of Extracellular Matrix Rigidity in 3D Tumor Models Using Particle-tracking Microrheology

Published on: June 10, 2014

Rheological transition driven by matrix makes cancer spheroids resilient under confinement.

Tavishi Dutt1, Jimpi Langthasa2, Monica Umesh2,3

  • 1Centre for Nanoscience and Engineering, Indian Institute of Science, Bangalore, India.

Life Science Alliance
|March 27, 2025
PubMed
Summary
This summary is machine-generated.

Ovarian cancer spheroids with a lumen and ECM coat (blastuloids) are more resilient than lumenless spheroids (moruloids). This mechanical difference, driven by E-cadherin, aids cancer cell survival in the peritoneal cavity.

More Related Videos

A Cancer Cell Spheroid Assay to Assess Invasion in a 3D Setting
05:34

A Cancer Cell Spheroid Assay to Assess Invasion in a 3D Setting

Published on: November 20, 2015

A 3D Spheroid Model as a More Physiological System for Cancer-Associated Fibroblasts Differentiation and Invasion In Vitro Studies
06:27

A 3D Spheroid Model as a More Physiological System for Cancer-Associated Fibroblasts Differentiation and Invasion In Vitro Studies

Published on: August 8, 2019

Related Experiment Videos

Last Updated: Jun 25, 2026

Longitudinal Measurement of Extracellular Matrix Rigidity in 3D Tumor Models Using Particle-tracking Microrheology
11:11

Longitudinal Measurement of Extracellular Matrix Rigidity in 3D Tumor Models Using Particle-tracking Microrheology

Published on: June 10, 2014

A Cancer Cell Spheroid Assay to Assess Invasion in a 3D Setting
05:34

A Cancer Cell Spheroid Assay to Assess Invasion in a 3D Setting

Published on: November 20, 2015

A 3D Spheroid Model as a More Physiological System for Cancer-Associated Fibroblasts Differentiation and Invasion In Vitro Studies
06:27

A 3D Spheroid Model as a More Physiological System for Cancer-Associated Fibroblasts Differentiation and Invasion In Vitro Studies

Published on: August 8, 2019

Area of Science:

  • Oncology
  • Biophysics
  • Cell Biology

Background:

  • Cancer metastasis involves disseminated cells forming spheroids within microenvironments.
  • Ovarian cancer spheroids often exhibit cavitation, forming blastuloid morphologies with an extracellular matrix (ECM) coat.
  • The mechanical properties of these spheroids influence their survival and dissemination.

Purpose of the Study:

  • To investigate how spheroidal morphology, specifically cavitation and ECM presence, affects mechanical integrity.
  • To understand the role of E-cadherin and intercellular adhesion in spheroid resilience.
  • To elucidate the mechanisms by which ovarian cancer spheroids survive in the peritoneal cavity.

Main Methods:

  • Atomic force microscopy to assess spheroid elasticity.
  • Microfluidic experiments to mimic peritoneal confinement and analyze cell flow and disintegration.
  • Computer simulations to model spheroid mechanics.
  • E-cadherin expression analysis and knockdown experiments.

Main Results:

  • Blastuloids (cavitated spheroids with ECM) were elastic, while moruloids (lumenless) were viscoplastic.
  • Moruloids showed greater disintegration and slower shape recovery in microfluidic flow compared to blastuloids.
  • ECM removal from blastuloids induced moruloid-like traits, including increased disintegration.
  • Higher E-cadherin expression correlated with blastuloid formation and resilience.

Conclusions:

  • The extracellular matrix and lumen formation are critical for spheroid transition from a labile to a resilient phenotype.
  • E-cadherin plays a key role in maintaining spheroid integrity and lumen formation.
  • These morphological and mechanical traits enhance cancer cell survival and facilitate metastasis within confined peritoneal flows.