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Related Concept Videos

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,...
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,...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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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...
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

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Transmitochondrial Cybrid Generation Using Cancer Cell Lines
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Reprogramming Proton-Coupled Electron Transfer in Living Cancer Cells to Eradicate Tumors.

Bo-Yu Wang1,2, Shun-Ran Peng3, Wei You3

  • 1Department of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China.

Journal of the American Chemical Society
|June 25, 2026
PubMed
Summary
This summary is machine-generated.

An organoiridium catalyst reprograms cancer cell metabolism by hijacking proton-coupled electron transfer (PCET). This artificial catalyst suppresses tumor growth by converting lactate production into hydrogen gas generation.

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Area of Science:

  • Biochemistry
  • Chemical Biology
  • Oncology

Background:

  • Intracellular proton-coupled electron transfer (PCET) is crucial for cellular metabolism and is dysregulated in diseases like cancer.
  • In cancer, lactate dehydrogenase (LDH) redirects PCET, promoting tumor growth, proliferation, and metastasis.
  • Targeting LDH-driven PCET is a potential antitumor strategy, but requires catalysts that can outcompete endogenous enzymes.

Purpose of the Study:

  • To develop an artificial catalyst capable of reprogramming intracellular PCET in living cancer cells.
  • To investigate if the catalyst can outcompete LDH and alter cancer cell metabolism.
  • To assess the therapeutic potential of PCET reprogramming for cancer treatment.

Main Methods:

  • An organoiridium catalyst, IrIII(Cp*)-CN, was synthesized and tested for its ability to capture electrons from NADH.
  • The catalyst's activity was evaluated in living cancer cells under ultrasound irradiation at physiological pH.
  • The study compared the catalyst's efficiency against endogenous LDH in redirecting PCET pathways.

Main Results:

  • IrIII(Cp*)-CN successfully captured proton-coupled electrons from NADH and transferred them to protons, generating H2.
  • In cancer cells, the catalyst outcompeted LDH, redirecting pyruvate reduction and lactate production towards H2 generation.
  • This reprogramming suppressed lactate and ATP production, significantly inhibiting tumor growth with low toxicity to normal tissues.

Conclusions:

  • Artificial catalysts can reprogram intracellular PCET by outcompeting endogenous enzymes like LDH.
  • PCET reprogramming offers a novel antitumor strategy by converting tumor-promoting pathways into tumor-suppressive ones.
  • This approach provides a framework for developing new treatments for diseases linked to aberrant cellular redox metabolism.