Related Experiment Video

Updated: Mar 30, 2026

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.5K

Palbociclib inhibits epithelial-mesenchymal transition and metastasis in breast cancer via c-Jun/COX-2 signaling

Ge Qin1, Fei Xu1, Tao Qin1

  • 1Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, China.

Oncotarget
|November 6, 2015
PubMed

Insights

Palbociclib, a CDK4/6 inhibitor, effectively reduces breast cancer metastasis by inhibiting epithelial-mesenchymal transition (EMT). This action is mediated through the c-Jun/COX-2 signaling pathway, offering new therapeutic insights.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Palbociclib is a selective inhibitor of cyclin-dependent kinases 4 and 6 (CDK4/6).
  • While effective against tumor proliferation, its role in preventing cancer metastasis is not fully understood.
  • Cancer metastasis remains a significant challenge in breast cancer treatment.

Purpose of the Study:

  • To investigate the anti-metastasis potential of palbociclib in breast cancer.
  • To elucidate the underlying molecular mechanisms regulating palbociclib's anti-metastasis activity.
  • To evaluate the impact of palbociclib on epithelial-mesenchymal transition (EMT) and related signaling pathways.

Main Methods:

  • In vitro studies using MDA-MB-231 and T47D breast cancer cell lines.
  • Analysis of epithelial-mesenchymal transition (EMT) markers (vimentin, Snail).
  • Investigation of the c-Jun/COX-2/PGE2 signaling pathway.
  • In vivo assessment of metastasis using bioluminescence imaging and tail vein injection models.

Main Results:

  • Palbociclib inhibited breast cancer cell migration and invasion.
  • Down-regulation of EMT markers (vimentin, Snail) was observed.
  • Palbociclib reduced c-Jun expression and its binding activity to the COX-2 promoter.
  • Decreased COX-2 and prostaglandin E2 (PGE2) production were noted.
  • In vivo studies confirmed reduced lung metastasis in palbociclib-treated mice.

Conclusions:

  • Palbociclib exhibits anti-metastasis effects in breast cancer by inhibiting EMT.
  • The anti-metastasis activity is mediated through the c-Jun/COX-2 signaling pathway.
  • These findings highlight palbociclib's potential as a therapeutic agent against breast cancer metastasis.
Keywords:
COX-2breast cancerepithelial-mesenchymal transitionmetastasispalbociclib

More Related Videos

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module10:39

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module

Published on: June 18, 2015

13.9K
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

8.1K

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
6.2K
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

5.6K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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...
6.3K
mTOR Signaling and Cancer Progression03:03

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...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.7K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
9.1K