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

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...
The Tumor Microenvironment02:17

The Tumor Microenvironment

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...
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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...

You might also read

Related Articles

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

Sort by
Same author

Modeling developmental spiking behavior driven by ionic current dynamics of mouse and human inner hair cells using a calcium-enhanced Izhikevich framework.

Journal of computational neuroscience·2026
Same author

Thrombin-PAR1 signaling regulates Topoisomerase 1 activity to bridge inflammation and breast cancer progression.

Cancer letters·2026
Same author

Pair production tomography enables imaging of MeV-scale gamma-emitting theranostic radionuclides.

Research square·2026
Same author

Harnessing Benzoyl-Urea Secondary-Sphere Hydrogen-Bonding to Enhance Oxygen Evolution Catalysis by Cobalt Corroles.

Small science·2026
Same author

Slow RNAPII elongation enhances naive pluripotency rewiring while maintaining high replication fork speed.

Science advances·2026
Same author

Sphingosine-1-phosphate promotes CD8 T cell exhaustion in breast cancer via exosomal transfer of TGFBR2.

Cell death & disease·2026

Related Experiment Video

Updated: May 19, 2026

Assessing Tumor Microenvironment of Metastasis Doorway-Mediated Vascular Permeability Associated with Cancer Cell Dissemination using Intravital Imaging and Fixed Tissue Analysis
09:42

Assessing Tumor Microenvironment of Metastasis Doorway-Mediated Vascular Permeability Associated with Cancer Cell Dissemination using Intravital Imaging and Fixed Tissue Analysis

Published on: June 26, 2019

Metabolic Cross Talk in the Tumor Microenvironment.

Chinmay Das1, Somya Ranjan Dash2, Biswajit Das3

  • 1School of Biotechnology, Kalinga Institute of Industrial Technology Deemed to be University, Bhubaneswar, Odisha, India.

Cancer Treatment and Research
|May 17, 2026
PubMed
Summary

Cancer cells and tumor microenvironment cells engage in metabolic crosstalk, reprogramming metabolism to fuel cancer progression and drug resistance. Understanding these interactions is key to developing new cancer therapies.

Keywords:
AutocrineDrug resistanceImmune infiltrationJuxtacrineMetabolic crosstalkMetabolic reprogrammingMetabolic vulnerabilitiesParacrineStromal and immune cellsTumor microenvironment (TME)Tumor progressionand endocrine signaling

More Related Videos

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

Related Experiment Videos

Last Updated: May 19, 2026

Assessing Tumor Microenvironment of Metastasis Doorway-Mediated Vascular Permeability Associated with Cancer Cell Dissemination using Intravital Imaging and Fixed Tissue Analysis
09:42

Assessing Tumor Microenvironment of Metastasis Doorway-Mediated Vascular Permeability Associated with Cancer Cell Dissemination using Intravital Imaging and Fixed Tissue Analysis

Published on: June 26, 2019

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

Area of Science:

  • Oncology
  • Cancer Biology
  • Metabolism

Background:

  • The tumor microenvironment (TME) comprises malignant, immune, stromal, endothelial cells, and the extracellular matrix.
  • Metabolic interactions within the TME significantly influence cancer progression, immune evasion, metastasis, and therapeutic resistance.

Purpose of the Study:

  • To provide a comprehensive overview of metabolic interactions between malignant and TME cells.
  • To highlight the role of key metabolites in TME communication.
  • To explore molecular mechanisms driving metabolic reprogramming in cancer.

Main Methods:

  • Literature review and synthesis of current research on TME metabolic crosstalk.
  • Analysis of autocrine, paracrine, juxtacrine, and endocrine-like communication pathways.
  • Examination of signaling pathways triggered by metabolite exchange.

Main Results:

  • Dynamic metabolic crosstalk within the TME supports cancer progression under stress conditions (hypoxia, acidosis).
  • Metabolic reprogramming of tumor-resident cells is crucial for cancer survival and growth.
  • Metabolite exchange between malignant and stromal cells promotes drug resistance.

Conclusions:

  • Metabolic interactions within the TME are critical drivers of cancer progression and drug resistance.
  • Targeting metabolic vulnerabilities in cancer cells presents a promising therapeutic strategy.
  • Understanding TME metabolic reprogramming is essential for novel cancer treatment development.