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

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.6K
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...
3.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.5K
1.5K
The Ras Gene02:38

The Ras Gene

5.7K
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...
5.7K
Mismatch Repair01:20

Mismatch Repair

5.4K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
5.4K
Mismatch Repair01:36

Mismatch Repair

37.9K
Overview
37.9K
Abnormal Proliferation02:23

Abnormal Proliferation

4.0K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.0K

You might also read

Related Articles

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

Sort by
Same author

tDNA(ser) sequences are involved in the excision of Streptomyces griseus plasmid pSG1.

Gene·1992
Same author

Expression of cytokines and their receptors by human thymocytes and thymic stromal cells.

Immunology·1992
Same author

Conservative surgery and radiation therapy for intraductal carcinoma of the breast.

The Journal of the Florida Medical Association·1992
Same author

Asymmetry in visual search for targets defined by differences in movement speed.

Journal of experimental psychology. Human perception and performance·1992
Same author

Clinical decision making for discharge planning in a changing psychiatric environment.

Health & social work·1992
Same author

Immunization of colorectal cancer patients with modified ovine submaxillary gland mucin and adjuvants induces IgM and IgG antibodies to sialylated Tn.

Cancer research·1992
Same journal

Correction: Neuropilin-1 promotes human glioma progression through potentiating the activity of the HGF/SF autocrine pathway.

Oncogene·2026
Same journal

Amphiregulin-mediated EGFR activation drives both intrinsic and acquired resistance to KRAS G12C inhibitors in KRAS G12C-mutant non-small cell lung cancer.

Oncogene·2026
Same journal

Histone lactylation-driven IGF2BP3 promotes intrahepatic cholangiocarcinoma progression via SPP1/CD44-dependent macrophage polarization.

Oncogene·2026
Same journal

Correction: SIRT7 activates p53 by enhancing PCAF-mediated MDM2 degradation to arrest the cell cycle.

Oncogene·2026
Same journal

Correction: Liver-specific SIRT1 knockout-induced hyperglycemia promotes spontaneous lung adenocarcinomas through HSF1-MDM2.

Oncogene·2026
Same journal

Correction: 6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 is essential for p53-null cancer cells.

Oncogene·2026
See all related articles

Related Experiment Video

Updated: Apr 27, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

945

MutT Homolog 1 (MTH1) maintains multiple KRAS-driven pro-malignant pathways.

A Patel1, D G A Burton1, K Halvorsen1

  • 1Department of Medicine, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.

Oncogene
|July 16, 2014
PubMed
Summary
This summary is machine-generated.

MutT Homolog 1 (MTH1) is crucial for KRAS-driven lung cancer progression by protecting cells from reactive oxygen species (ROS). Inhibiting MTH1 halts tumor growth and may offer a new therapeutic strategy for KRAS-mutant non-small cell lung carcinoma.

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 Cancer
06:51

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

18.9K
Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

8.6K

Related Experiment Videos

Last Updated: Apr 27, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

945
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

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

18.9K
Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

8.6K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Oncogenic RAS proteins elevate reactive oxygen species (ROS), which paradoxically promote malignancy while also triggering tumor suppression.
  • RAS-driven cancer cells necessitate robust redox-protective mechanisms to counteract ROS-induced damage.
  • MutT Homolog 1 (MTH1), an 8-oxodGTPase, plays a key role in mitigating oxidative damage within the nucleotide pool.

Purpose of the Study:

  • To investigate the role of MTH1 in maintaining pro-malignant traits driven by KRAS mutations in non-small cell lung carcinoma (NSCLC).
  • To elucidate the molecular mechanisms by which MTH1 influences KRAS-driven oncogenesis and tumor progression.

Main Methods:

  • Utilized a non-small cell lung carcinoma (NSCLC) model with KRAS mutations.
  • Performed MTH1 suppression experiments in KRAS-mutant NSCLC cells and immortalized lung epithelial cells.
  • Analyzed MTH1 expression in human NSCLC tumors and correlated it with KRAS levels.
  • Investigated the impact of MTH1 loss on DNA damage, senescence, proliferation, and KRAS expression in p53-competent and p53-nonfunctional cells.

Main Results:

  • MTH1 suppression impaired proliferation and xenograft tumor formation in KRAS-mutant NSCLC cells.
  • MTH1 levels were found to modulate KRAS-induced cellular transformation.
  • MTH1 expression was upregulated by oncogenic KRAS and positively correlated with KRAS levels in human NSCLC.
  • In p53-competent cells, MTH1 loss induced DNA damage and senescence; in p53-nonfunctional cells, it reduced proliferation and KRAS expression.

Conclusions:

  • MTH1 is essential for sustaining KRAS-driven pro-malignant phenotypes in NSCLC.
  • MTH1 functions not only in preventing oxidative DNA damage but also in regulating oncogene expression levels.
  • MTH1 represents a critical component in KRAS-associated malignancy, suggesting its inhibition as a potential therapeutic strategy for KRAS-driven tumors.