Researchers Identify Metabolic Pathway Allowing Cancer Cells to Accumulate Iron

Turning off a specific mitochondrial complex that seemed to buffer iron-induced cell death revealed few side effects in mice.

Key Highlights

  • Researchers discovered a key metabolic pathway that allows colorectal cancer cells to accumulate large amounts of iron, promoting their growth.
  • Blocking this pathway caused cancer cells to die, indicating a promising target for future treatments.
  • Mitochondrial complex II plays a crucial role in protecting tumor cells from iron toxicity by regulating coenzyme Q.
  • Knocking out complex II in mouse models resulted in few side effects, suggesting potential for safe therapeutic interventions.
  • The study highlights multiple mechanisms, including cellular heme and mitochondrial regulation, that cancer cells use to survive iron-related stress.

Michigan Medicine researchers have discovered a key metabolic pathway that "allows colorectal cancer cells to accumulate large quantities of iron."

Blocking the pathway in question caused the cancer cells to die. Cancer cells accumulate even higher amounts of iron as they become more aggressive, which stands in opposition to normal cells with high levels of iron, which "undergo a type of iron-related cell death called ferroptosis."

Researchers conducted a metabolism-focused CRISPR screen that ended up revealing "cellular heme, an iron-containing molecule, was protecting tumor cells against iron toxicity." They discovered a specific mitochondrial complex, complex II, was "buffering iron-induced cell death by regulating coenzyme Q."

When complex II was knocked out in mouse models, the researchers observed "few side effects." This could make for a promising target in the fight against colorectal cancer. Iron itself was also observed to regulate complex II, which could imply multiple ways to break the cycle to be researched further.

About the Author

Matt MacKenzie

Associate Editor

Matt is Associate Editor for Healthcare Purchasing News.

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