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Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

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...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Electron Transport Chain: Complex III and IV01:43

Electron Transport Chain: Complex III and IV

During the electron transport chain, electrons from NADH and FADH2 are first transferred to complexes I and II, respectively. These two complexes then transfer the electrons to ubiquinol, which carries them further to complex III. Complex III passes the electrons across the intermembrane space to Cyt c, which carries them further to complex IV. Complex IV donates electrons to oxygen and reduces it to water. As electrons pass through complexes I, III, and IV, the energy released aids the pumping...
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,...
The Electron Transport Chain01:30

The Electron Transport Chain

The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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...

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Related Experiment Video

Updated: May 29, 2026

Revealing the Ferroptotic Phenotype of Medulloblastoma
04:01

Revealing the Ferroptotic Phenotype of Medulloblastoma

Published on: March 15, 2024

Iron-addicted colorectal cancers exploit heme-complex II axis to resist oxidative cell death.

Chesta Jain1, Muqit Essani1, Roshan Kumar2

  • 1University of Michigan, Department of Molecular & Integrative Physiology, Ann Arbor, MI, USA.

Cell Metabolism
|May 27, 2026
PubMed
Summary

Colorectal cancer cells exploit iron for growth but can be vulnerable. A new heme-succinate dehydrogenase (SDH)-coenzyme Q (CoQ) axis helps them survive high iron by detoxifying oxidative stress, revealing potential therapeutic targets.

Keywords:
colorectal canceriron toxicitymitochondrial antioxidantoxidative stress

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Quantifiable and Inexpensive Cell-Free Fluorescent Method to Confirm the Ability of Novel Compounds to Chelate Iron
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Quantifiable and Inexpensive Cell-Free Fluorescent Method to Confirm the Ability of Novel Compounds to Chelate Iron

Published on: February 23, 2024

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Last Updated: May 29, 2026

Revealing the Ferroptotic Phenotype of Medulloblastoma
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Quantifiable and Inexpensive Cell-Free Fluorescent Method to Confirm the Ability of Novel Compounds to Chelate Iron
05:36

Quantifiable and Inexpensive Cell-Free Fluorescent Method to Confirm the Ability of Novel Compounds to Chelate Iron

Published on: February 23, 2024

Area of Science:

  • Biochemistry
  • Cell Biology
  • Cancer Research

Background:

  • Colorectal cancer (CRC) cells exhibit high iron dependency for proliferation and metabolism.
  • High intracellular iron is typically cytotoxic, yet CRC cells thrive in iron-rich environments.
  • The role of ferroptosis regulators in modulating iron toxicity in vivo remains largely unknown.

Purpose of the Study:

  • To investigate the mechanisms by which colorectal cancer cells tolerate and exploit iron-rich conditions.
  • To identify key molecular pathways involved in buffering iron-induced oxidative stress in CRC.
  • To uncover novel therapeutic vulnerabilities in colorectal cancer metabolism.

Main Methods:

  • Multi-omics profiling of colorectal cancer cells.
  • CRISPR screening to identify genetic dependencies.
  • In vivo model studies to assess iron toxicity and cellular responses.
  • Biochemical assays to analyze the heme-succinate dehydrogenase (SDH)-coenzyme Q (CoQ) axis.

Main Results:

  • A novel heme-succinate dehydrogenase (SDH)-coenzyme Q (CoQ) axis was identified in CRC cells.
  • This axis enables CRC cells to buffer iron-induced oxidative stress.
  • Heme-dependent SDH reduces CoQ, which acts as a radical-trapping antioxidant at cellular membranes.
  • CRC cells co-opt metabolic pathways for both growth and survival under high iron conditions.

Conclusions:

  • Colorectal cancer cells possess a unique metabolic adaptation involving the SDH-CoQ axis to manage iron toxicity.
  • This axis allows CRC cells to utilize iron for growth while mitigating its cytotoxic effects.
  • Targeting this metabolic axis presents a potential therapeutic strategy for colorectal cancer.