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

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

You might also read

Related Articles

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

Sort by
Same author

Case Report: Pulmonary alveolar adenoma: a case series from a single institution and literature review.

Frontiers in oncology·2026
Same author

MAPPING THE MTOR PATHWAY IN LUNG TRANSPLANTATION: IS IT TIME FOR A BIOMARKER-DRIVEN PRECISION THERAPY?

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation·2026
Same author

CHIMERA: A Phase II Study of Neoadjuvant Pembrolizumab in Combination With Cisplatin or Carboplatin and Pemetrexed Followed by Surgery and Adjuvant Pembrolizumab in Resectable Pleural Mesothelioma.

Clinical lung cancer·2026
Same author

Use of a composite, 3D-printed patch as a partial airway replacement: A pilot study on the porcine model.

Bioengineering & translational medicine·2026
Same author

International Society for Heart and Lung Transplantation Scientific Statement on pulmonary antibody-mediated rejection and proposed graft, antibody, and pathology (GAP) definition.

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation·2026
Same author

A Perspective Summary of the ISHLT Consensus Statement on Acute Lung Allograft Dysfunction (ALAD).

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation·2026

Related Experiment Video

Updated: Jun 12, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

SERPINB3 induces epithelial-mesenchymal transition.

Santina Quarta1, Laura Vidalino, Cristian Turato

  • 1Department of Clinical and Experimental Medicine, University of Padova, Italy.

The Journal of Pathology
|June 8, 2010
PubMed
Summary

The study shows that SERPINB3 protein promotes cancer cell invasion by triggering epithelial-mesenchymal transition (EMT). This process enhances tumor cell migration and metastasis, highlighting SERPINB3 as a potential therapeutic target.

More Related Videos

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

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

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

Related Experiment Videos

Last Updated: Jun 12, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

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

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Epithelial-mesenchymal transition (EMT) is crucial for tumor invasion and metastasis.
  • SERPINB3, a serine protease inhibitor, is over-expressed in epithelial tumors and inhibits apoptosis.

Purpose of the Study:

  • To investigate the role of SERPINB3 in modulating EMT and its impact on cancer cell invasion.
  • To determine the autocrine and paracrine effects of SERPINB3 on tumor cell behavior.

Main Methods:

  • Morphological, molecular, and cell biology techniques were used on HepG2 cell clones transfected with SERPINB3.
  • Paracrine effects were assessed using exogenous recombinant SERPINB3 on HepG2 and MDCK cell lines.
  • Ultrastructural analysis and gene expression studies were performed.

Main Results:

  • SERPINB3 expression altered cell morphology, reduced desmosomal junctions, and increased intercellular spaces.
  • E-cadherin decreased while beta-catenin and vimentin increased, indicating EMT.
  • SERPINB3 induced cell scattering, migration, invasiveness, and colony formation in soft agar, independent of protease activity.

Conclusions:

  • SERPINB3 promotes EMT, leading to increased cell invasiveness and metastasis potential.
  • SERPINB3 acts through both autocrine and paracrine mechanisms.
  • These findings suggest SERPINB3 is a key player in tumor progression and a potential therapeutic target.