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

Alternative RNA Splicing02:18

Alternative RNA Splicing

21.0K
Alternative RNA splicing is the regulated splicing of exons and introns to produce different mature mRNAs from a single pre-mRNA. Unlike in constitutive splicing where a single gene produces a single type of mRNA, alternative splicing allows an organism to produce multiple proteins from a single gene and plays an important role in protein diversity.
There are five types of alternative RNA splicing that vary in the ways the pre-mRNA segments are removed or retained in the mature mRNA. The first...
21.0K
RNA Splicing01:32

RNA Splicing

56.1K
Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...
56.1K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
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...
4.5K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.8K
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...
3.8K
Epigenetic Regulation01:37

Epigenetic Regulation

3.0K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.0K
RNA Editing02:23

RNA Editing

8.9K
RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...
8.9K

You might also read

Related Articles

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

Sort by
Same author

A U1-U3 snRNA-snoRNA interaction couples SF3B1 mutation to chromatin-state rewiring and genome instability.

bioRxiv : the preprint server for biology·2026
Same author

Left and Right Heart Remodelling at 1 Year After Transcatheter Versus Surgical Aortic Valve Replacement: A Speckle-Tracking Echocardiography Study.

Interdisciplinary cardiovascular and thoracic surgery·2026
Same author

Reply to "A Re-discussion of the Definitions of the Onset and End of Atrial Strains".

Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography·2026
Same author

One-Year Outcomes of Screen Failures for Transcatheter Tricuspid Valve Repair: Insights From the TriSelect Study.

Circulation. Cardiovascular interventions·2026
Same author

Postoperative 4-chamber cardiac function and outcomes following biatrial or left atrial Maze procedure for concomitant atrial fibrillation.

JTCVS open·2026
Same author

Left Ventricular Myocardial Work Indices and Mechanical Dispersion in an Elite Basketball Athlete Population.

The American journal of cardiology·2026

Related Experiment Video

Updated: Jun 11, 2025

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
10:06

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Published on: April 26, 2017

8.9K

APC mutations dysregulate alternative polyadenylation in cancer.

Austin M Gabel1,2,3,4, Andrea E Belleville1,2,3,5, James D Thomas1,2

  • 1Computational Biology Program, Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, WA, USA.

Genome Biology
|October 7, 2024
PubMed
Summary

Loss of the APC gene disrupts alternative polyadenylation (APA) in colorectal cancer, leading to widespread gene expression changes. This finding reveals a new mechanism driving cancer development.

More Related Videos

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
11:48

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Published on: October 9, 2014

12.9K
Identification of Alternative Splicing and Polyadenylation in RNA-seq Data
08:35

Identification of Alternative Splicing and Polyadenylation in RNA-seq Data

Published on: June 24, 2021

5.5K

Related Experiment Videos

Last Updated: Jun 11, 2025

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
10:06

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Published on: April 26, 2017

8.9K
Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
11:48

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Published on: October 9, 2014

12.9K
Identification of Alternative Splicing and Polyadenylation in RNA-seq Data
08:35

Identification of Alternative Splicing and Polyadenylation in RNA-seq Data

Published on: June 24, 2021

5.5K

Area of Science:

  • Genomics
  • Molecular Biology
  • Cancer Research

Background:

  • Alternative polyadenylation (APA) is a common gene regulation mechanism affecting most human genes.
  • APA dysregulation is a hallmark of many cancers, but its underlying causes are not fully understood.

Purpose of the Study:

  • To investigate the molecular regulators of poly(A) site selection across various cancer types.
  • To understand the specific role of Adenomatous Polyposis Coli (APC) mutations in APA dysregulation, particularly in colorectal adenocarcinoma.

Main Methods:

  • Unbiased analysis of poly(A) site selection regulators using The Cancer Genome Atlas (TCGA) data.
  • Comparative analysis of APA in colorectal adenocarcinoma versus other cancer subtypes.
  • Experimental validation using human colon organoids with APC knockout.
  • Bioinformatic analysis of existing APC eCLIP data to identify binding motifs.

Main Results:

  • Colorectal adenocarcinoma exhibits distinct APA patterns compared to other cancers, linked to frequent APC loss-of-function mutations.
  • APC mutations are associated with longer 3' UTR expression, indicating a shift towards distal polyadenylation site usage.
  • APC knockout in colon organoids recapitulates APA dysregulation observed in tumors.
  • APC protein preferentially binds G- and C-rich motifs upstream of proximal poly(A) sites.
  • Reduced APC expression correlates with APA dysregulation even in cancers without recurrent APC mutations.

Conclusions:

  • APC acts as a regulator of proximal poly(A) site usage.
  • APC loss or altered expression contributes significantly to the pervasive APA dysregulation observed in various cancers.
  • These findings highlight APC's role in maintaining normal gene expression through APA regulation and its implications in cancer pathogenesis.