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

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
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

4.3K
4.3K
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
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

19.5K
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...
19.5K
Regulation of Metabolism01:19

Regulation of Metabolism

12.3K
Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
12.3K

You might also read

Related Articles

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

Sort by
Same author

A live cell biosensor protocol for high-resolution screening of therapy-resistant cancer cells.

PloS one·2026
Same author

Small Extracellular Vesicles From Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response.

Journal of extracellular vesicles·2025
Same author

A live cell biosensor protocol for high-resolution screening of therapy-resistant cancer cells.

bioRxiv : the preprint server for biology·2025
Same author

A high-throughput workflow for assessing self-renewal using colony formation assays.

Stem cell research·2025
Same author

Small Extracellular Vesicles from Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response.

bioRxiv : the preprint server for biology·2025
Same author

The PACT Network: PRL, ARL, CNNM, and TRPM Proteins in Magnesium Transport and Disease.

International journal of molecular sciences·2025

Related Experiment Video

Updated: Mar 29, 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

3.3K

NHE1-Mediated Metabolic Reprogramming in Cancer.

Majd A Al-Hamaly1,2, Beau R Forester2,3, Jessica S Blackburn2,3

  • 1Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY 40356, USA.

Metabolites
|March 27, 2026
PubMed
Summary
This summary is machine-generated.

The sodium-hydrogen exchanger-1 (NHE1) transporter is crucial for cancer cell metabolism and growth. Targeting NHE1 offers potential new cancer therapies by disrupting cancer cell metabolic reprogramming.

Keywords:
NHE1OXPHOScancer metabolismion exchangersmitochondriapH regulation

More Related Videos

Assessment of the Metabolic Profile of Primary Leukemia Cells
06:21

Assessment of the Metabolic Profile of Primary Leukemia Cells

Published on: November 21, 2018

11.1K

Related Experiment Videos

Last Updated: Mar 29, 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

3.3K
Assessment of the Metabolic Profile of Primary Leukemia Cells
06:21

Assessment of the Metabolic Profile of Primary Leukemia Cells

Published on: November 21, 2018

11.1K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Physiology

Background:

  • Sodium-hydrogen exchanger-1 (NHE1) is a transmembrane transporter vital for cellular pH homeostasis.
  • NHE1 is frequently overexpressed in various cancers, correlating with metastasis and proliferation.
  • Emerging research highlights NHE1's role in regulating cancer cell metabolism.

Purpose of the Study:

  • To review the current evidence linking NHE1 dysregulation to metabolic reprogramming in cancer.
  • To focus on NHE1's influence on mitochondrial metabolism, glycolytic flux, lysosomal biology, and oxidative stress pathways.
  • To evaluate pharmacological strategies targeting NHE1 for cancer treatment.

Main Methods:

  • Literature review synthesizing current research on NHE1 and cancer metabolism.
  • Analysis of studies investigating NHE1's impact on metabolic pathways and cellular functions.
  • Evaluation of clinical data and challenges associated with NHE1-targeting drugs.

Main Results:

  • NHE1 dysregulation significantly impacts cancer cell metabolism, including mitochondrial function and redox balance.
  • NHE1 drives intracellular alkalinization, influencing the tumor microenvironment and metabolic pathways.
  • Targeting NHE1 affects metabolic reprogramming, with potential therapeutic benefits but also clinical limitations.

Conclusions:

  • NHE1 acts as an integrator of ion transport and metabolic control in cancer.
  • Targeting NHE1-driven metabolic programs presents a promising avenue for novel cancer therapeutics.
  • Further research and clinical development are needed to overcome challenges in applying NHE1 inhibitors.