Related Experiment Video

Updated: May 27, 2026

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

Carnosine inhibits KRAS-mediated HCT116 proliferation by affecting ATP and ROS production

Barbara Iovine1, Maria Luigia Iannella, Francesca Nocella

  • 1Dipartimento di Biochimica e Biotecnologie Mediche, Università di Napoli "Federico II", 80131 Napoli, Italy.

Cancer Letters
|December 6, 2011
PubMed

Insights

Carnosine, a natural antioxidant, effectively inhibits human colon cancer cell growth by reducing ATP and ROS levels. This antiproliferative effect is linked to cell cycle arrest and modulation of key signaling proteins.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Carnosine is a naturally occurring dipeptide with known antioxidant and anti-aging properties.
  • Its antiproliferative potential, particularly in cancer, is an area of growing research interest.
  • Activating KRAS mutations in HCT116 colon cancer cells are known to induce mitochondrial reactive oxygen species (ROS), promoting proliferation.

Purpose of the Study:

  • To investigate the antiproliferative effects of carnosine on human HCT116 colon cancer cells.
  • To elucidate the underlying molecular mechanisms, including the impact on cellular energy and signaling pathways.

Main Methods:

  • Treatment of HCT116 colon cancer cells with varying concentrations of carnosine (50-100 mM).
  • Measurement of intracellular ATP and ROS levels.
  • Cell cycle analysis to determine phase distribution.
  • Western blot analysis to assess ERK1/2 phosphorylation and p21waf1 protein expression.

Main Results:

  • Carnosine significantly inhibited the proliferation of HCT116 colon cancer cells.
  • Treatment led to a dose-dependent decrease in ATP and ROS concentrations.
  • Carnosine induced cell cycle arrest at the G1 phase.
  • These effects were associated with reduced ERK1/2 phosphorylation and increased p21waf1 protein levels.

Conclusions:

  • Carnosine exhibits significant antiproliferative activity against HCT116 colon cancer cells.
  • The mechanism involves carnosine's antioxidant properties, reduction of cellular ATP, and modulation of cell cycle regulatory proteins.
  • Carnosine's impact on glycolysis may also contribute to its anti-cancer effects, suggesting therapeutic potential.

More Related Videos

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein07:08

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein

Published on: January 16, 2020

Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...
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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
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,...