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

Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

10.0K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
10.0K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

2.9K
2.9K
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

65
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
65
Tumor Progression02:07

Tumor Progression

7.8K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
7.8K
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

13.9K
As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
13.9K

You might also read

Related Articles

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

Sort by
Same author

Lumbosacral spinal cord epidural stimulation improves voiding function after human spinal cord injury.

Scientific reports·2018
Same author

Family Experiences with the Diagnosis of Autism Spectrum Disorder: System Barriers and Facilitators of Efficient Diagnosis.

Journal of autism and developmental disorders·2018
Same author

Minimally invasive wireless motility capsule to study canine gastrointestinal motility and pH.

Veterinary journal (London, England : 1997)·2017
Same author

Interleukin-22 drives nitric oxide-dependent DNA damage and dysplasia in a murine model of colitis-associated cancer.

Mucosal immunology·2017
Same author

Effect of home-based light treatment on persons with dementia and their caregivers.

Lighting research & technology (London, England : 2001)·2015
Same author

Ajuga turkestanica increases Notch and Wnt signaling in aged skeletal muscle.

European review for medical and pharmacological sciences·2014

Related Experiment Video

Updated: Mar 19, 2026

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

7.1K

Myeloid translocation genes differentially regulate colorectal cancer programs.

B Parang1,2, A M Bradley1,2, M K Mittal1,2

  • 1Department of Medicine, Division of Gastroenterology, Vanderbilt University School of Medicine, Nashville, TN, USA.

Oncogene
|June 9, 2016
PubMed
Summary

Loss of Myeloid Translocation Gene 1 (MTGR1) promotes intestinal tumorigenesis by increasing cell proliferation and activating Wnt and Notch signaling. MTGR1 downregulation is observed in human colorectal cancer.

More Related Videos

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

10.1K
Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer
06:19

Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer

Published on: July 18, 2017

10.9K

Related Experiment Videos

Last Updated: Mar 19, 2026

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

7.1K
A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

10.1K
Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer
06:19

Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer

Published on: July 18, 2017

10.9K

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Myeloid translocation genes (MTGs) are transcriptional corepressors involved in hematopoietic stem cell regulation.
  • MTGs, including MTGR1 and MTG16, have potential roles in epithelial malignancies.
  • Loss of function of MTGs may promote tumorigenesis.

Purpose of the Study:

  • To investigate the role of MTGR1 and MTG16 in intestinal epithelial homeostasis and tumorigenesis.
  • To determine the impact of MTGR1 and MTG16 loss on Apc-dependent intestinal tumor development.
  • To explore the molecular mechanisms underlying MTGR1's role in colorectal cancer.

Main Methods:

  • Genetic deletion of MTGR1 and MTG16 in mice.
  • Analysis of Apc1638/+-dependent intestinal tumorigenesis models.
  • Chromatin immunoprecipitation sequencing (ChIP-seq) to identify MTGR1 and MTG16 targets.
  • Immunohistochemistry and gene expression analysis of Wnt and Notch signaling pathways.
  • Analysis of The Cancer Genome Atlas (TCGA) and human colorectal cancer (CRC) samples.

Main Results:

  • Mtgr1-/- mice exhibited progressive depletion of intestinal secretory cells and increased epithelial cell proliferation.
  • Mtgr1-/- mice showed a 10-fold increase in intestinal tumor multiplicity, advanced dysplasia, and invasive adenocarcinoma.
  • Loss of MTGR1 led to hyperactivation of Wnt and Notch signaling pathways in tumors.
  • MTGR1 was downregulated at both transcript and protein levels in human colorectal cancer samples.

Conclusions:

  • MTGR1 plays a critical role in maintaining intestinal epithelial homeostasis.
  • Loss of MTGR1 promotes intestinal tumorigenesis through Wnt and Notch signaling hyperactivation.
  • MTGR1 acts as a tumor suppressor in the context of intestinal epithelial malignancies.
  • MTGR1's context-dependent function suggests a complex role in tumorigenesis.