Related Experiment Video

Updated: Nov 21, 2025

The Use of Mouse Mammary Tumor Cells in an In Vitro Invasion Assay as a Measure of Oncogenic Cell Behavior
08:12

The Use of Mouse Mammary Tumor Cells in an In Vitro Invasion Assay as a Measure of Oncogenic Cell Behavior

Published on: June 12, 2019

5.3K

TIMELESS inhibits breast cancer cell invasion and metastasis by down-regulating the expression of MMP9

Bowen Li1, Liying Mu1, Yanan Li1

  • 1School of Bioengineering & Key Laboratory of Protein Modification and Disease, Liaoning Province, Dalian University of Technology, 2 Ling Gong Road, Dalian, 116024, Liaoning, China.

Cancer Cell International
|January 12, 2021
PubMed

Insights

The TIMELESS protein inhibits breast cancer cell invasion and metastasis by reducing MMP9 expression. It achieves this by preventing p65 acetylation and blocking the NF-κB signaling pathway, crucial for tumor spread.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Breast cancer remains a leading cause of female mortality, with metastasis being a primary driver of patient death.
  • The precise molecular mechanisms underlying breast cancer metastasis are not fully elucidated.
  • Identifying novel therapeutic targets to inhibit metastasis is critical.

Purpose of the Study:

  • To investigate the role of TIMELESS in breast cancer cell invasion and metastasis.
  • To elucidate the molecular mechanisms by which TIMELESS affects breast cancer progression.
  • To explore the potential of targeting TIMELESS for breast cancer treatment.

Main Methods:

  • Overexpression and knockdown of TIMELESS in ZR-75-30 breast cancer cells.
  • Assessment of cell invasion and metastasis assays.
  • Analysis of F-actin assembly, MMP9 mRNA and protein levels.
  • Investigation of TIMELESS interaction with p65 and CBP.
  • Evaluation of p65 acetylation and NF-κB pathway activation.

Main Results:

  • Overexpression of TIMELESS significantly inhibited breast cancer cell invasion, metastasis, and F-actin assembly.
  • Knockdown of TIMELESS promoted breast cancer cell invasion and metastasis.
  • TIMELESS overexpression led to decreased MMP9 expression at both mRNA and protein levels.
  • TIMELESS interacted with p65, inhibiting its acetylation by CBP and suppressing NF-κB pathway activation.

Conclusions:

  • TIMELESS acts as a suppressor of breast cancer cell invasion and metastasis.
  • The TIMELESS-mediated inhibition involves down-regulation of MMP9 expression via the p65/NF-κB pathway.
  • TIMELESS represents a potential therapeutic target for inhibiting breast cancer metastasis.
Keywords:
Breast cancerInvasionMMP9MetastasisTIMELESS

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

13.5K
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

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

Published on: June 9, 2023

1.9K

Related Concept Videos

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...
6.1K
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...
5.3K
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...
4.1K