Research

The overarching goal of my laboratory is to understand the molecular mechanisms of tumor progression and metastasis. We have played a major role in establishing the current models of non-coding RNA regulation of epithelial-mesenchymal transition, metastasis, and therapy resistance. Moreover, we discovered the deubiquitinases for key cancer proteins; some of these deubiquitinases are promising therapeutic targets.

Currently, our team is: (1) establishing new paradigms for RNA functions and mechanisms (non-coding RNAs, RNA epigenetics, and RNA-binding proteins) in tumor progression and metastasis; (2) screening for deubiquitinating enzymes that promote tumorigenesis, metastasis, and therapy resistance; (3) investigating novel regulators and regulations of tumor radioresistance and drug resistance; and (4) studying the role of specific developmental regulators in cancer, metabolism, and regeneration by using genetically engineered mouse models generated in our lab.

The Ma Laboratory's Five Most Important Contributions in the Past Four Years

1. Through targeted inactivation, restoration (genetic rescue), and overexpression of MALAT1 in multiple in vivo models (genetically engineered mouse models, xenograft models, and syngeneic models), the The Ma Laboratory demonstrated that the lncRNA MALAT1 suppresses breast cancer metastasis through binding and inactivation of the pro-metastatic transcription factor TEAD (Nature Genetics 2018, last and corresponding author).

2. The Ma Laboratory discovered a novel mechanism by which non-proteolytic ubiquitination promotes YAP nuclear localization and activity, and identified the ubiquitin E3 ligase and the deubiquitinase that regulate this ubiquitination (Nature Communications 2018, last and corresponding author).

3. The Ma Laboratory identified an ovarian tumor protease (OTU) family member as an EZH2 deubiquitinase and a potential therapeutic target in breast cancer (Cell Reports 2018, last and corresponding author).

4. The Ma Laboratory generated miR-10b knockout mice and found that genetic deletion of miR-10b suppressed oncogene-induced mammary tumorigenesis, EMT, and metastasis and reactivated tumor-suppressive pathways (Cancer Research 2016, last and corresponding author).

5. Dr. Ma collaborated with TCGA Research Network and made key contributions to integrated genomic analysis of the ubiquitin pathway across many cancer types (Cell Reports 2018, second last author).