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

Abnormal Proliferation02:23

Abnormal Proliferation

5.1K
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...
5.1K
Rab Cascades01:25

Rab Cascades

3.4K
Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
3.4K
Rab Proteins01:14

Rab Proteins

4.9K
Rab proteins constitute the largest family of monomeric GTPases, of which 70 members are present in humans. Rab proteins and their effectors regulate consecutive stages of vesicle transport such as vesicle transport, docking, and fusion to the correct recipient membrane.
Rab proteins switch between a cytosolic, GDP-bound inactive state and a membrane-anchored, GTP-bound active state. By themselves, Rabs show slow rates of GDP/GTP exchange and GTP hydrolysis. Thus, Rab proteins are considered...
4.9K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

2.7K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.7K
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

3.2K
Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
3.2K
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

3.4K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
3.4K

You might also read

Related Articles

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

Sort by
Same author

Gli2-serpinh1 drives fibroblast state transition during skin wound healing.

NPJ Regenerative medicine·2026
Same author

Toward system-level integration of organoids for regenerative medicine.

Burns & trauma·2026
Same author

Nocturnal Respiratory Rate and Variability Predict Long-term Mortality in Stable Outpatients with Cardiovascular Disease.

medRxiv : the preprint server for health sciences·2026
Same author

Examining the impact on quality-of-life of those living with inherited optic neuropathies: an updated systematic review.

Canadian journal of ophthalmology. Journal canadien d'ophtalmologie·2026
Same author

The Ecological Relationship Between Food Access and Disease Activity in Canadian Children Newly Diagnosed With Juvenile Idiopathic Arthritis.

The Journal of rheumatology·2026
Same author

A modified angular spectrum method for rapid on-demand design of axisymmetric acoustic metalenses.

The Journal of the Acoustical Society of America·2026

Related Experiment Video

Updated: Jan 11, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

19.1K

Pannexin 1 induces Rhabdomyosarcoma cell fusion by downregulating APOBEC2.

Alexandra Welten1,2, Amit Bera1, Stéphanie Langlois1,3

  • 1Molecular Biomedicine Program, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada.

Oncogenesis
|November 18, 2025
PubMed
Summary

Pannexin 1 (PANX1) suppresses rhabdomyosarcoma (RMS) by downregulating APOBEC2, promoting cell fusion. Restoring APOBEC2 levels blocks this PANX1-induced fusion, offering therapeutic insights for RMS cancer.

More Related Videos

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

9.8K
Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes
11:01

Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes

Published on: August 24, 2021

3.3K

Related Experiment Videos

Last Updated: Jan 11, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

19.1K
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

9.8K
Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes
11:01

Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes

Published on: August 24, 2021

3.3K

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Rhabdomyosarcoma (RMS) is an aggressive cancer linked to faulty muscle development (myogenesis).
  • Pannexin 1 (PANX1) shows potential in overcoming RMS, but its mechanism is unclear.
  • APOBEC2 (apolipoprotein B mRNA editing enzyme catalytic subunit 2) is a myogenic modulator downregulated by PANX1 in RMS.

Purpose of the Study:

  • To investigate the role of APOBEC2 in PANX1-mediated suppression of RMS.
  • To understand how PANX1 affects APOBEC2 levels and RMS cell behavior.
  • To explore the link between PANX1, APOBEC2, and cell fusion in RMS.

Main Methods:

  • RNA-sequencing (RNA-seq) to analyze transcriptomic changes.
  • Analysis of patient-derived RMS cell lines and tumor specimens.
  • Overexpression studies of PANX1 and APOBEC2 in RMS cells.

Main Results:

  • APOBEC2 levels are lower in RMS compared to normal muscle cells.
  • APOBEC2 promotes stem-like characteristics and spheroid growth in RMS cells.
  • PANX1 overexpression downregulates APOBEC2 and triggers multinucleation via cell fusion in RMS.
  • Restoring APOBEC2 inhibits PANX1-induced cell fusion while preserving other anti-tumor effects.

Conclusions:

  • PANX1 promotes RMS cell fusion by reducing APOBEC2 expression.
  • This downregulation drives RMS cells towards a myogenic program.
  • Targeting the PANX1-APOBEC2 pathway may offer new therapeutic strategies for RMS.