Area of research
Molecular Biology · Cancer Research
Research interest
Research focused on Cancer research and Breast cancer, with related work in Triple-negative breast cancer, Cancer, PI3K/AKT/mTOR pathway. Notable publications include 'Hypoxic tumor microenvironment activates GLI2 via HIF-1α and TGF-β2 to promote chemoresistance in colorectal cancer', 'Chromosome 1q21.3 amplification is a trackable biomarker and actionable target for breast cancer recurrence', and 'PDK1 Signaling Toward PLK1–MYC Activation Confers Oncogenic Transformation, Tumor-Initiating Cell Activation, and Resistance to mTOR-Targeted Therapy'.
Assessment of the potential impact of polymorphisms in the Foxp3 and CTLA-4 genes in immune balance and disease susceptibility of primary Sjögren’s syndrome
Administration of necrostatin-1 ameliorates glucocorticoid-induced osteonecrosis of the femoral head in rats
Altered Fecal Metabolomics and Potential Biomarkers of Psoriatic Arthritis Differing From Rheumatoid Arthritis
Stromal induction of BRD4 phosphorylation Results in Chromatin Remodeling and BET inhibitor Resistance in Colorectal Cancer
The relationship between common variants in the <i>DPEP1</i> gene and the susceptibility and clinical severity of osteoarthritis
Oral treatment with glycyrrhizin inhibits NLRP3 inflammasome activation and promotes microglial M2 polarization after traumatic spinal cord injury
Metformin attenuates bleomycin-induced scleroderma by regulating the balance of Treg/Teff cells and reducing spleen germinal center formation
Hypoxic tumor microenvironment activates GLI2 via HIF-1α and TGF-β2 to promote chemoresistance in colorectal cancer
KDM6B Counteracts EZH2-Mediated Suppression of <i>IGFBP5</i> to Confer Resistance to PI3K/AKT Inhibitor Treatment in Breast Cancer
Necrostatin-1 inhibits the cell death of osteoblasts induced by glucocorticoid.
PubMed 2018cited by 8position: first
Chromosome 1q21.3 amplification is a trackable biomarker and actionable target for breast cancer recurrence
HIFI-α activation underlies a functional switch in the paradoxical role of Ezh2/PRC2 in breast cancer
Endoplasmic reticulum stress of Kupffer cells involved in the conversion of natural regulatory T cells to Th17 cells in liver ischemia‐reperfusion injury
RASAL2 activates RAC1 to promote triple-negative breast cancer progression
PDK1 Signaling Toward PLK1–MYC Activation Confers Oncogenic Transformation, Tumor-Initiating Cell Activation, and Resistance to mTOR-Targeted Therapy
Protein tyrosine phosphatase <i>UBASH3B</i> is overexpressed in triple-negative breast cancer and promotes invasion and metastasis