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

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

6.5K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.5K
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

8.7K
The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
8.7K
Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

7.3K
Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
7.3K
MicroRNAs01:22

MicroRNAs

3.0K
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
3.0K
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
Metastasis02:30

Metastasis

5.5K
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...
5.5K
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Mir-200-mediated Inactivation Of Cancer-associated Fibroblasts Via Targeting Of Nrp2-vegfr Signaling Attenuates Lung Cancer Invasion And Metastasis.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Mir-200-mediated Inactivation Of Cancer-associated Fibroblasts Via Targeting Of Nrp2-vegfr Signaling Attenuates Lung Cancer Invasion And Metastasis.

Related Experiment Video

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

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

9.4K

miR-200-mediated inactivation of cancer-associated fibroblasts via targeting of NRP2-VEGFR signaling attenuates lung cancer invasion and metastasis.

Inyoung Cheon1, Sieun Lee1, Seonyeong Oh1

  • 1Department of Molecular Medicine and Inflammation-Cancer Microenvironment Research Center, College of Medicine, Ewha Womans University, Seoul 07804, Korea.

Molecular Therapy. Nucleic Acids
|May 20, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

MicroRNA-200 (miR-200) inhibits cancer-associated fibroblasts (CAFs) from promoting lung cancer progression. This microRNA targets NRP2, offering potential therapeutic strategies for lung cancer treatment.

Keywords:
MT: Non-coding RNAsNRP2cancer-associated fibroblastsinvasiveness

More Related Videos

Isolation of Primary Cancer-Associated Fibroblasts from a Syngeneic Murine Model of Breast Cancer for the Study of Targeted Nanoparticles
08:02

Isolation of Primary Cancer-Associated Fibroblasts from a Syngeneic Murine Model of Breast Cancer for the Study of Targeted Nanoparticles

Published on: May 14, 2021

5.6K
The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
07:39

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues

Published on: June 16, 2018

9.3K

Related Experiment Videos

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

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

9.4K
Isolation of Primary Cancer-Associated Fibroblasts from a Syngeneic Murine Model of Breast Cancer for the Study of Targeted Nanoparticles
08:02

Isolation of Primary Cancer-Associated Fibroblasts from a Syngeneic Murine Model of Breast Cancer for the Study of Targeted Nanoparticles

Published on: May 14, 2021

5.6K
The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
07:39

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues

Published on: June 16, 2018

9.3K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cancer-associated fibroblasts (CAFs) significantly contribute to tumor progression, including motility, drug resistance, angiogenesis, and metastasis.
  • Understanding CAF activation mechanisms is crucial for developing effective cancer therapies.

Purpose of the Study:

  • To investigate whether microRNA-200 (miR-200), a known suppressor of epithelial-mesenchymal transition, can inhibit CAFs from promoting lung cancer progression.
  • To identify the molecular targets and pathways through which miR-200 exerts its effects on CAFs.

Main Methods:

  • Overexpression of miR-200 in CAFs.
  • Assays to evaluate lung cancer cell migration, invasion, tumorigenicity, and metastasis.
  • Assessment of CAF-mediated effects on macrophage polarization and vascular endothelial cell function.
lung cancer
miR-200
  • Confirmation of NRP2 as a direct target of miR-200 using molecular techniques.
  • Analysis of NRP2-VEGFR signaling pathway components, including VEGF-D and pleiotrophin secretion.

    • Main Results:

    • Overexpression of miR-200 significantly inhibited lung cancer cell migration, invasion, tumorigenicity, and metastasis.
    • miR-200 suppressed CAF-induced recruitment and M2 polarization of macrophages.
    • miR-200 impaired the migration and tube formation of vascular endothelial cells.
    • NRP2 was identified as a direct target of miR-200, mediating its functional effects in CAFs.
    • miR-200 inhibition of the NRP2-VEGFR pathway reduced VEGF-D and pleiotrophin secretion, thereby suppressing cancer cell invasion.

    Conclusions:

    • miR-200 effectively remodels CAFs to impede lung cancer progression and metastasis.
    • The miR-200/NRP2 axis represents a promising therapeutic target for lung cancer treatment.