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

4.7K
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...
4.7K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

6.6K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.6K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

4.1K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.1K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

5.0K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.0K

You might also read

Related Articles

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

Sort by
Same author

Fibroblast growth factor 23 inhibition attenuates steroid-induced osteonecrosis of the femoral head through pyroptosis.

Scientific reports·2024
Same author

Fibroblast growth factor 23 regulates hypoxia‑induced osteoblast apoptosis through the autophagy‑signaling pathway.

Molecular medicine reports·2023
Same author

FGF23 promotes proliferation, migration and invasion by regulating miR-340-5p in osteosarcoma.

Journal of orthopaedic surgery and research·2023
Same author

SIRT6 Prevents Glucocorticoid-Induced Osteonecrosis of the Femoral Head in Rats.

Oxidative medicine and cellular longevity·2022
Same author

lncRNA FGD5-AS1 Regulates Bone Marrow Stem Cell Proliferation and Apoptosis by Affecting miR-296-5p/STAT3 Axis in Steroid-Induced Osteonecrosis of the Femoral Head.

Journal of healthcare engineering·2022
Same author

Mental Health and Behavioral Outcomes of Sexual and Nonsexual Child Maltreatment Among Child Welfare-Involved Youth.

Journal of child sexual abuse·2016

Related Experiment Video

Updated: Oct 7, 2025

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
08:07

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Published on: April 12, 2019

7.3K

Interfering with pak4 Protein Expression Affects Osteosarcoma Cell Proliferation and Migration.

Yuxin Fu1, Lun Fang1, Qipu Yin1

  • 1Institute of Sports Medicine, Shandong First Medical University & Shandong Academy Medical Sciences, 619 Changcheng Road, Taian, 271016 Shandong, China.

Biomed Research International
|January 10, 2022
PubMed
Summary

This study investigated the role of PAK4 in osteosarcoma, finding that PAK4 protein expression significantly impacts cancer cell proliferation and migration. Interfering with PAK4 affects osteosarcoma progression.

More Related Videos

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
04:25

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models

Published on: October 28, 2021

10.1K
A Preclinical Mouse Model of Osteosarcoma to Define the Extracellular Vesicle-mediated Communication Between Tumor and Mesenchymal Stem Cells
11:15

A Preclinical Mouse Model of Osteosarcoma to Define the Extracellular Vesicle-mediated Communication Between Tumor and Mesenchymal Stem Cells

Published on: May 6, 2018

10.3K

Related Experiment Videos

Last Updated: Oct 7, 2025

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
08:07

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Published on: April 12, 2019

7.3K
Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
04:25

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models

Published on: October 28, 2021

10.1K
A Preclinical Mouse Model of Osteosarcoma to Define the Extracellular Vesicle-mediated Communication Between Tumor and Mesenchymal Stem Cells
11:15

A Preclinical Mouse Model of Osteosarcoma to Define the Extracellular Vesicle-mediated Communication Between Tumor and Mesenchymal Stem Cells

Published on: May 6, 2018

10.3K

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • The role of PAK4 in human tumors is recognized, but its specific function and mechanisms in osteosarcoma remain unclear.
  • Understanding PAK4's involvement is crucial for developing targeted osteosarcoma therapies.

Purpose of the Study:

  • To investigate the effect of PAK4 on osteosarcoma cell proliferation and migration.
  • To elucidate the underlying molecular mechanisms of PAK4 in osteosarcoma.

Main Methods:

  • Quantitative real-time PCR (QRT-PCR) and Western blot were used to measure PAK4 protein and mRNA levels.
  • Cellular viability and mobility were assessed using MTT and wound-healing assays.
  • Adenovirus-mediated overexpression and liposome-mediated knockout were employed to manipulate PAK4 levels.

Main Results:

  • Overexpression of PAK4 stimulated proliferation and migration in U2-OS and MG-63 osteosarcoma cells.
  • Knockout of PAK4 inhibited osteosarcoma cell proliferation.
  • PAK4 expression positively correlated with cell cycle regulators (P21, CyclinD1, CyclinE1, CDK2, CDK6), promoting G0/G1 to G2/M phase transition.
  • PAK4 activated Erk expression and induced epithelial-mesenchymal transition (EMT) in osteosarcoma cells.

Conclusions:

  • PAK4 plays a significant role in regulating osteosarcoma cell proliferation and migration.
  • Modulating PAK4 protein expression presents a potential therapeutic strategy for osteosarcoma.