Our primary research interests focus on erbB receptor tyrosine kinases (RTKs)-mediated signal transduction in breast cancer and noncoding RNA (ncRNA)-mediated epigenetic regulation of drug resistance and metastasis. By understanding the molecular basis of RTK signaling in tumorigenesis and ncRNA, including miRNA and lncRNA, regulation of tumor progression, we hope to identify novel targets and develop epigenetic approaches with therapeutic potential for cancer treatment.
There are currently three areas of investigation in my laboratory:
Project 1: Role of erbB3 signaling in cancer drug resistance and tumor metastasis. Our recent data show that the erbB3 signaling exerts its biologic function via regulation of two tumor suppressive miRNAs, miR-203 and miR-542-3p. Modern molecular and cellular biology techniques are applied to determine how miR-203 and miR-542-3p contribute to erbB3-mediated drug resistance and tumor metastasis.
Project 2: Identification of novel erbB3-targeted therapy. Our ongoing studies aim to determine whether the novel strategy/agents targeting of erbB3 (cooperative miRNAs and epigenetic modulators) may abrogate or attenuate the therapeutic resistance to tamoxifen, paclitaxel, and/or trastuzumab against erbB2-overexpressing (erbB2+) breast cancer.
Project 3: Epigenetic enhancement of chemotherapy against non-small cell lung cancer (NSCLC), multiple myeloma (MM), acute myeloid leukemia (AML). We have discovered that the HDAC inhibitors, such as entinostat, panobinostat, and SAHA are able to induce expression of tumor suppressive miRNAs and lncRNAs, leading to downregulation of Survivin and several key EMT markers, respectively. Our studies suggest that ncRNA-mediated epigenetic approach is a useful strategy to significantly potentiate chemotherapeutic agents-induced antitumor activity.