Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Abnormal Proliferation

Abnormal Proliferation

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...

mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

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...

Tumor Progression

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...

TGF - β Signaling Pathway

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...

Interactions Between Signaling Pathways

Interactions Between Signaling Pathways

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...

The Retinoblastoma Gene

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...

You might also read

Related Articles

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

Sort by

Same author

The extracellular regulatory network and key factors governing early embryogenesis in Nicotiana tabacum.

Plant & cell physiology·2026

Same author

A straightforward approach for converting existing batch production to an integrated continuous manufacturing suite by adopting membrane-based technology.

Biotechnology progress·2026

Same author

Enhanced photodynamic inactivation against Listeria monocytogenes under blue light mediated by carbon dots derived from 'Shatian' pomelo peels for ready-to-eat sausage preservation.

International journal of food microbiology·2026

Same author

Plasticizer-responsive molecular axes in heart failure: a subtype-aware toxicogenomic framework relevant to environmental health.

Environment international·2026

Same author

Development of a novel GAK solution for efficient hypothermic preservation of NK cell viability and anti-tumor function.

Stem cell research & therapy·2026

Same author

Exploring subclinical median nerve biomechanical changes in elderly rheumatoid arthritis patients with nerve ultrasound and shear wave elastography: a cross-sectional study.

Scientific reports·2026

Search research articles

Related Experiment Video

Updated: Dec 8, 2025

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

Published on: May 3, 2021

p38γ overexpression promotes osteosarcoma cell progression.

Ce Shi^1,2, Wei-Nan Cheng³, Yin Wang⁴

¹Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.

|September 24, 2020

Summary

This summary is machine-generated.

p38 gamma (p38γ) is overexpressed in osteosarcoma (OS), a common adolescent bone cancer. Inhibiting p38γ slows OS cell growth, migration, and invasion, suggesting it

Keywords:

molecularly targeted therapy osteosarcoma p38γ

More Related Videos

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

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

Published on: October 28, 2021

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Published on: April 12, 2019

Related Experiment Videos

Last Updated: Dec 8, 2025

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

Published on: May 3, 2021

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

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

Published on: October 28, 2021

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Published on: April 12, 2019

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

Osteosarcoma (OS) is the most frequent primary bone cancer in adolescents.
p38 gamma (p38γ) kinase activity is implicated in promoting cell cycle progression and tumorigenesis through retinoblastoma (Rb) phosphorylation.
The role of p38γ in human OS progression requires further elucidation.

Purpose of the Study:

To investigate the expression and function of p38γ in human osteosarcoma.
To determine the impact of p38γ modulation on OS cell behavior and underlying molecular mechanisms.

Main Methods:

Quantitative analysis of p38γ mRNA and protein in OS tissues and cells versus normal bone and osteoblasts.
Functional assays including cell growth, proliferation, migration, invasion, and apoptosis.
Gene manipulation techniques such as shRNA knockdown, CRISPR/Cas9 knockout, and ectopic overexpression of p38γ.
Western blot analysis to assess Rb phosphorylation and cyclin E1/A expression.

Main Results:

p38γ expression is significantly elevated in human OS tissues and cells compared to normal counterparts.
p38γ knockdown or knockout markedly inhibited OS cell growth, proliferation, migration, and invasion, while enhancing apoptosis.
Ectopic p38γ overexpression promoted OS cell growth, proliferation, and migration.
Modulation of p38γ levels directly affected Rb phosphorylation and cyclin E1/A expression, key regulators of cell cycle progression.

Conclusions:

p38γ is a critical driver of human osteosarcoma progression.
Elevated p38γ expression promotes OS cell proliferation, migration, and invasion by regulating Rb phosphorylation and cell cycle-related gene expression.
p38γ represents a potential therapeutic target for osteosarcoma treatment.