Mission statement

The Naba lab studies the role of the extracellular matrix (ECM) in development, health, and disease, with a particular focus on cancer. To do so, we utilize classical molecular, cellular, and developmental biology approaches in combination with cutting-edge proteomics and computational analyses. Our goal is to better understand how the ECM contributes to diseases so that we can exploit it to develop novel diagnostic and therapeutic strategies. 

The Naba lab is a highly collaborative and dynamic group that strives for scientific excellence, and offers a stimulating and inclusive working environment conducive to learning and professional development.

Research Projects

The extracellular matrix (ECM), a complex meshwork of cross-linked proteins, is a fundamental components of multicellular organisms. It provides architectural supports to the cells, confers mechanical properties to tissues, and conveys biochemical signals transduced by cell surface receptors to control various cellular processes such as proliferation, survival, differentiation, adhesion and migration.
Alterations in the composition and organization of the ECM cause or accompany the development of diseases such as fibrosis, cardio-vascular diseases, and cancer.

To explore the importance of the ECM in diseases, we have previously developed, in the context of the Matrisome Project, proteomic and bioinformatic approaches to study the molecular composition of the ECM, or the "matrisome" of normal and diseased tissues.
Using these approaches, we discovered that:
1) the ECM of any given tissue is composed of 150+ different proteins
2) the composition of the ECM varies i) between tissues, ii) between normal tissues and tumors arising from them, iii) between tumors of different metastatic potentials, and iv) between primary tumors and their distant metastases.

Projects currently ongoing in the lab include:

Project 1: Understanding the role of SNED1, a novel extracellular matrix protein in development, health, and disease.
We previously identified a novel ECM protein, SNED1 (Sushi, Nidogen and EGF-like domain protein 1), in a proteomic screen aimed at discovering ECM proteins differentially expressed between highly and poorly metastatic mammary tumors. We reported that SNED1 was produced only by highly metastatic tumor cells, and not by poorly metastatic tumor cells or by stromal cells, and that it played a functional role in tumor dissemination, as, SNED1 knockdown decreased metastasis in a murine model of breast cancer. We further showed that the level of expression of SNED1 was a prognostic factor for hormone-negative breast cancer patients (Naba et al., eLife, 2014).
  • Role of SNED1 in breast cancer metastasis:
We now wish to 1) pinpoint which steps of the metastatic cascade are dependent on SNED1, 2) dissect the cellular and molecular mechanisms controlled by SNED1 and contributing to cancer progression, and 3) further evaluate the prognostic value of SNED1's expression for human cancer patients.
  • Role of SNED1 in normal development:
The importance of SNED1 in breast cancer metastasis prompted us to evaluate the role of SNED1 in normal development and physiology. To do so, we generated a mouse model lacking Sned1 and are currently studying the impact of Sned1 deletion on whole-organism development.

Project 2: Development of  quantitative proteomic approaches to study the role of the ECM in metastatic tropism and response to anti-cancer therapies.
  • Role of the ECM in metastatic tropism and the formation of metastatic niches:

Metastatic tropism is defined as the preferential dissemination of certain primary tumors to certain organs, termed secondary sites. For example, breast cancers will preferentially disseminate to lung, liver, brain and bones, whereas colon cancers will preferentially metastasize to the liver. We are hypothesizing that the ECM of primary and/or secondary tumors contribute to determining metastatic tropism and will be using label-based quantitative proteomics to address this question.

  • Role of the ECM in response to anti-cancer therapies:
We are interested in addressing the following questions:
How does the composition of the tumor ECM change in response to anti-cancer therapies?
Can we derive prognostic signatures distinguishing tumors that will or not respond to treatment?
Are ECM proteins causal of resistance? If so, can we interfere with ECM-mediated resistance?