Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Cancer-Critical Genes II: Tumor Suppressor Genes

Cancer-Critical Genes II: Tumor Suppressor Genes

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...

Cancer-Critical Genes II: Tumor Suppressor Genes

Cancer-Critical Genes II: Tumor Suppressor Genes

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...

Cancer-Critical Genes I: Proto-oncogenes

Cancer-Critical Genes I: Proto-oncogenes

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...

Cancer-Critical Genes I: Proto-oncogenes

Cancer-Critical Genes I: Proto-oncogenes

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...

Adaptive Mechanisms in Cancer Cells

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 Cells

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,...

You might also read

Related Articles

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

Sort by

Same author

Envelope-Limited Chromatin Sheets (ELCS) Formation in The Nuclear Envelope of HL-60/S4 Cells.

bioRxiv : the preprint server for biology·2026

Same author

Mitochondria as a Therapeutic Target for Burn Injury.

Biomolecules·2026

Same author

Impaired mitochondrial stress signaling mediates bone loss in male mice in the absence of BNIP3.

bioRxiv : the preprint server for biology·2026

Same author

Nuclear Pore Complexes in Various States of HL-60/S4 Cells.

bioRxiv : the preprint server for biology·2026

Same author

Deletion of <i>Dock7</i> Exons 3 and 4 Results in Reduced Trabecular Microarchitecture and a Decrease in Mineralization.

bioRxiv : the preprint server for biology·2026

Same author

Beyond <i>mecA</i>: a two-tiered mechanism and regulatory rewiring drive high-level ceftaroline resistance in clinical MRSA.

Antimicrobial agents and chemotherapy·2026

Search research articles

Related Experiment Video

Updated: Jun 6, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Two novel human NUMB isoforms provide a potential link between development and cancer.

Aldona Karaczyn¹, Mahmud Bani-Yaghoub, Roger Tremblay

¹Center for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, ME 04074, USA.

Neural Development

|December 3, 2010

Summary

Two new NUMB isoforms, NUMB5 and NUMB6, were identified. They are linked to cancer and alter cell migration by interacting with CDC42 and affecting NOTCH signaling.

More Related Videos

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Published on: May 17, 2024

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Published on: April 26, 2017

Related Experiment Videos

Last Updated: Jun 6, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Published on: May 17, 2024

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Published on: April 26, 2017

Area of Science:

Cell Biology
Molecular Biology
Oncology

Background:

The NUMB protein regulates cell polarity and fate by antagonizing NOTCH signaling.
Four human NUMB isoforms have been previously identified, each with distinct functions.

Purpose of the Study:

To identify and characterize novel human NUMB isoforms.
To investigate the role of these new isoforms in cell migration and cancer.

Main Methods:

Reverse transcription-polymerase chain reaction (RT-PCR) and luciferase assays to assess NOTCH signaling antagonism.
Immunocytochemistry to analyze protein interactions.
Ectopic expression studies to observe effects on cell morphology and migration.
In vitro and in vivo migration assays.

Main Results:

Two novel NUMB isoforms, NUMB5 and NUMB6, lacking exon 10, were identified.
NUMB5 and NUMB6 exhibit reduced antagonism of NOTCH signaling compared to other isoforms.
These isoforms interact with CDC42, vimentin, and IQGAP1.
Ectopic expression of NUMB5 and NUMB6 induces lamellipodia and filopodia formation, respectively, in a CDC42- and RAC1-dependent manner.
NUMB5 and NUMB6 alter cell migratory behavior.

Conclusions:

NUMB5 and NUMB6 represent novel regulators of cell polarity and migration.
Their altered interaction with NOTCH signaling and association with CDC42 suggest a role in cancer progression.
These findings provide new insights into NUMB function in development and disease.