Related Experiment Video

Updated: Apr 14, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

14.9K

Targeting matriptase in breast cancer abrogates tumour progression via impairment of stromal-epithelial growth factor

Gina L Zoratti1, Lauren M Tanabe2, Fausto A Varela2

  • 11] Department of Pharmacology, Wayne State University School of Medicine and Barbara Ann Karmanos Cancer Institute, 540 E Canfield, Scott Hall Room 6332, Detroit, Michigan 48201, USA [2] Department of Oncology, Wayne State University School of Medicine and Barbara Ann Karmanos Cancer Institute, 540 E Canfield, Scott Hall Room 6332, Detroit, Michigan 48201, USA [3] Cancer Biology Graduate Program, Wayne State University School of Medicine and Barbara Ann Karmanos Cancer Institute, 110 E. Warren Avenue, Suite 2215, Detroit, Michigan 48201, USA.

Nature Communications
|April 16, 2015
PubMed

Insights

Matriptase, a protease, is crucial for breast cancer growth by activating the c-Met pathway. Inhibiting matriptase may offer a new therapeutic strategy for breast cancer treatment.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Matriptase is an epithelial-specific serine protease.
  • Its dysregulation is observed in various epithelial cancers, including breast cancer.
  • Reduced matriptase levels in mice delay mammary tumor formation and growth.

Purpose of the Study:

  • To investigate the role of matriptase in breast cancer cell proliferation.
  • To elucidate the mechanism by which matriptase influences cancer cell growth.
  • To evaluate matriptase as a potential therapeutic target for breast cancer.

Main Methods:

  • Genetic deletion and silencing of matriptase in breast cancer cells.
  • Inhibition of matriptase catalytic activity using a small-molecule inhibitor.
  • Analysis of c-Met signaling pathway activation in response to pro-HGF.

Main Results:

  • Matriptase-deficient breast cancer cells exhibit impaired proliferation.
  • This impairment is due to the inability to activate the c-Met signaling pathway.
  • Inhibition of matriptase abrogates c-Met, Gab1, and AKT activation, leading to reduced proliferation.

Conclusions:

  • Matriptase is essential for activating the c-Met pathway in response to pro-HGF.
  • Matriptase plays a critical role in breast cancer progression.
  • Matriptase represents a promising therapeutic target for breast cancer.

More Related Videos

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

2.5K
An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation08:48

An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation

Published on: June 30, 2015

8.7K

Related Concept Videos

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

1.8K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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...
8.5K
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...
9.2K
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...
6.5K
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
8.2K