We are investigating the effect of exosomes, a group of extracellular vesicles (EVs), from virus infected cells on cancer progression, inflammation and co-infection. We are utilizing the "EV-omics", including proteomics, RNAseq, lipidomics and metabolics to identify exosomes cargoes that contribute to diseases. We are also developing exosome therapeutic techniques in cancer treatment and regenerative medicine.
Teaching Information
Courses Taught
Research Information
Research Projects
Dr. Ge Jin’s research focuses on identifying signals sent out by tumor cells that recruit and activate tumor-promoting immune cells, particularly tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), for cancer progression. His laboratory has discovered that human β-defensin-3 (hBD3), a secreted epithelial cell-derived protein, is overexpressed in and released by oral precancerous lesions and oral cancer cells at the invasive front, while production of hBD1 and hBD2 are reduced. Further studies in Dr. Jin’s laboratory has found that tumor cell-derived hBD3 is involved in TAM accumulation using the chemokine receptor CCR2 and stimulates macrophages to produce chemokines and cytokines, potentially forming a positive feedback loop driving tumor progression.
In addition, his laboratory has identified that hBD3 production is driven by activation of growth factor receptors and inactivation of tumor suppressors, defined signaling networks previously identified to direct head and neck carcinogenesis. Dr. Jin’s laboratory recently finds that high-risk human papillomaviruses (HPVs), which are involved the progression of a subset of head and neck cancer, induce production of hBD3 through the tumor suppressor. Most recently, Dr. Jin is working on an NIH sponsored project to investigate the immune response and potential immunotherapeutic targets of head and neck cancer. He has been collaborating with researchers in the Department and with members of the Case Comprehensive Cancer Center to develop biomarkers of head and neck cancer and other solid tumors.
Recent Funding
Head Neck Cancer, beta-Defensins, and Immune Responses – R01
Role: Principal Investigator
Sponsor: NIH-NIDCR
Project Period: 07/2015 – 06/2020
Innate Immunity and Oral Carcinogenesis – R56
Role: Principal Investigator
Sponsor: NIH-NIDCR
Project Period: 7/2011 – 6/2012
Human β-defensins as Novel Biomarkers for Precancerous Lesions of Colorectal Cancer – Pilot Grant
Role: Principal Investigator
Sponsor: Case Compressive Cancer Center
Project Period: 4/2011 – 3/2012
Biomarkers of Human Papillomavirus-associated Head and Neck cancer
Role: Principal Investigator
Sponsor: STERIS Corporation
Funding Period: 8/2011 – 7/2012
Role of Human β-defensin-3 in the Progression of Tumors – Pilot Grant
Role: Principal Investigator
Sponsor: American Cancer Society
Project Period: 9/2009 – 8/2010
Functional Genomic Screen of the Transforming Growth Factor-β Signaling Molecules – SDG
Role: Principal Investigator
Sponsor: American Heart Association
Funding Period: 7/2005 – 6/2009
Publications
Kawsar HI, Weinberg A, Hirsch SA, Venizelos A, Howell S, Jiang B, Jin G, Overexpression of human β-defensin-3 in oral dysplasia: Potential role in macrophage trafficking. Oral Oncol. 45 (7):696-702 (2009).
Jin G, Kawsar HI, Hirsch SA, Zeng C, Jia X, Feng Z, Ghosh SK, Zheng QY, Zhou A, McIntyre TM, Weinberg A. An antimicrobial peptide regulates tumor-associated macrophage trafficking via the chemokine receptor CCR2, a model for tumorigenesis. PLoS One. 5 (6): e10993 (2010).
Chaudhury A, Hussey GS, Ray PS, Jin G, Fox PL, and Howe PH. TGFβ-mediated phosphorylation of hnRNP E1 induces EMT via transcript-selective translational induction of Dab2 and ILEI. Nat. Cell Biol. 12 (3): 286-293 (2010).
Jin G. Using biomarkers to detect oral cancer holds potential for saving lives when the cancer is most curable. Biomark Med. 4(6): 835-838 (2010).
Kawsar HI, Ghosh SK, Hirsch SA, Koon HB, Weinberg A, and Jin G. Expression of human β-defensin-2 in intratumoral vascular endothelium and in endothelial cells induced by transforming growth factor-β. Peptides. 31 (2): 195-201 (2010).