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

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

19.6K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
19.6K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.9K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.9K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

7.4K
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,...
7.4K
Replicative Cell Senescence02:15

Replicative Cell Senescence

4.6K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
4.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

5.1K
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...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.7K
1.7K

You might also read

Related Articles

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

Sort by
Same author

Mitochondrial double-stranded RNA fuels pancreatic cancer growth via RIG-I/TLR3 inflammation.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by small molecules.

Cell reports·2025
Same author

Androgen Receptors Promote Oxidative Phosphorylation and Resistance to Palmitate Lipotoxicity in ER-Mutant Breast Cancer.

Endocrinology·2025
Same author

Parkin Induces Ubiquitination and Large Extracellular Vesicle Release of HMGB1 to Activate Antitumor Immunity.

Cancer research·2025
Same author

eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by novel small molecules.

bioRxiv : the preprint server for biology·2025
Same author

Kaposi's sarcoma-associated herpesvirus induces mitochondrial fission to evade host immune responses and promote viral production.

Nature microbiology·2025

Related Experiment Video

Updated: Apr 4, 2026

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

3.4K

Disabling mitochondrial reprogramming in cancer.

M Cecilia Caino1, Dario C Altieri1

  • 1Prostate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, United States.

Pharmacological Research
|September 15, 2015
PubMed
Summary
This summary is machine-generated.

Molecular therapy with PI3K antagonists causes tumor cells to move mitochondria, increasing invasion. This highlights mitochondrial roles in cancer metabolism and offers new therapeutic targets to prevent metastasis.

Keywords:
Drug resistanceHsp90MetastasisMitochondriaPI3K

More Related Videos

An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model
06:05

An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model

Published on: March 9, 2022

4.6K
An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity
07:58

An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity

Published on: May 12, 2020

7.6K

Related Experiment Videos

Last Updated: Apr 4, 2026

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

3.4K
An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model
06:05

An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model

Published on: March 9, 2022

4.6K
An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity
07:58

An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity

Published on: May 12, 2020

7.6K

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • PI3K antagonists are used in molecular cancer therapy.
  • Tumor cells exhibit altered mitochondrial distribution under certain therapies.
  • Mitochondrial function is crucial for cancer cell behavior.

Purpose of the Study:

  • To investigate the impact of PI3K antagonists on tumor cell mitochondria.
  • To understand how mitochondrial redistribution affects tumor cell invasion.
  • To explore therapeutic opportunities related to mitochondrial bioenergetics in cancer.

Main Methods:

  • Exposure of tumor cells to PI3K antagonists.
  • Microscopy to observe mitochondrial redistribution.
  • Analysis of cell motility and invasion assays.

Main Results:

  • PI3K antagonist treatment caused mitochondria to relocate to the cell periphery.
  • This redistribution supported increased membrane dynamics and focal adhesion turnover.
  • Enhanced tumor cell motility and invasion were observed.

Conclusions:

  • Mitochondrial redistribution is a key response to PI3K antagonist therapy.
  • Regional mitochondrial bioenergetics plays a critical role in tumor metabolic reprogramming.
  • Targeting mitochondrial function presents a therapeutic strategy to combat cancer metastasis.