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Home   Researchers   Our researchers
Prof John Hooper

Prof John Hooper

Email

john.hooper@mater.uq.edu.au

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    Prof John Hooper

    Professor John Hooper is a Mater Foundation Fellow and a Senior Research Fellow at Mater Research. John leads the Cancer Cell Biology Research Group and is the author of over 70 publications with his research currently focused on understanding molecular mechanisms underlying cancer.

    John’s lab has a particular interest in aggressive malignancies, including cancers of the prostate, colon/rectum, pancreas and ovary, and works closely with Mater clinicians to identify key areas of need in these malignancies, with an ongoing emphasis on the role in cancer of cell surface receptor systems. The lab’s work is underpinned by molecular, enzymology and cell biology approaches, analysis of human tissues and pre-clinical models of cancer to identify cancer promoting molecular pathways and to test new anti-cancer drugs.

    Since 2010, John has helped to drive the establishment of gynaecological, urological and breast cancer research teams at the Mater Hospitals. These are closely aligned with Mater’s clinical multidisciplinary teams and involve surgeons, medical oncologists, pathologists, palliative care physicians, nurses and basic researchers.

    John is grateful for the more than $6.5 million in research funding that has supported his research from a range of agencies including the National Health & Medical Research Council (NHMRC), Mater Foundation, the Australian Research Council, Cancer Council Queensland, the Wesley Research Institute and The Prostate Cancer Foundation of Australia.

    ‘My research focus on cancer continues to be motivated by an innate drive to understand the aberrant molecular interactions that cause cells to grow, move and survive in settings where they would normally die. My goal is to develop novel therapies that modulate these interactions in such a way that they result in cancer cell death, tumour regression and improved patient survival and quality of life.’

    Research Programs and Groups

    • Cancer Biology and Care - Cancer Cell Biology Research

    Research Interests

    • Cancer Cell Biology - Oncology and Carcinogenesis
    • Cancer Diagnosis - Oncology and Carcinogenesis

    Projects

    • A novel protease and growth factor regulated signalling system in ovarian cancer. - Team Role: Principal Investigator

    Funding

    • 2016 - Brisbane Diamantina Health Partners (Strategic Initiative Grant Scheme) - $45,000.00
      Funded ProjectThe Queensland Gynaecological Cancer Initiative
    • 2015 - University of Queensland (Queensland Emory Development Alliance (QED)) - $60,420.00
      Funded ProjectTargeting Epigenetic modifying enzymes in aggressive cancers
    • 2015 - University of Queensland (Uniquest - AstraZeneca) - $76,020.00
      Funded ProjectRepurposing an Aurora B inhibitor and a myeloperoxidase inhibitor for serous ovarian cancer
    • 2015 - University of Queensland (UQ-Ochsner Seed Fund for Collaborative Research) - $22,500.00
      Funded ProjectThe role of cancer stem cells in colorectal cancer metastasis: Phase II – identifying therapeutic strategies
    • 2014 - Cancer Council Queensland (Project Grant) - $200,000.00
      Funded ProjectMacrophages facilitate prostate cancer bone metastasis
    • 2014 - Cancer Council Queensland (Project Grant) - $200,000.00
      Funded ProjectTargeting CDCP1 to reduce tumour burden and ascites in clear cell ovarian cancer
    • 2014 - Cancer Council Qld (Project Grant) - $0.00
      Funded ProjectTargeting CDCP1 to reduce tumour burden and ascites in clear cell ovarian cancer
    • 2014 - Cancel Council Qld (Project Grant) - $0.00
      Funded ProjectMacrophages facilitate prostate cancer bone metastasis
    • 2013 - ARC (Equipment Grant) - $0.00
      Funded ProjectMicro-ultrasound plus LAZR Photoacoustic Imaging Platform
    • 2013 - National Health and Medical Research Council (Project Grant) - $430,504.50
      Funded ProjectCharacterisation of novel hormone receptors
    • 2012 - Cancer Council Queensland (Project Grant) - $199,782.00
      Funded ProjectTargeting Inflammatory Pathways in Epithelial Ovarian Cancers
    • 2012 - Cancer Council Queensland (Project Grant) - $200,000.00
      Funded ProjectA novel Src regulated protease activated signalling pathway in hematogenous metastasis
    • 2012 - Cancer Council Qld (Project Grant) - $0.00
      Funded ProjectA novel Src regulated protease activated signalling pathway in hematogenous metastasis
    • 2012 - NHMRC (Project Grant) - $0.00
      Funded ProjectNovel reagents for treating iron disorders
    • 2011 - Australian Research Council (Future Fellowship) - $0.00
      Funded Project
    • 2011 - Cancer Council Qld (Project Grant) - $0.00
      Funded ProjectA novel molecular pathway in cancer
    • 2011 - Australian Research Council (Future Fellowship) - $822,856.00
      Funded ProjectA new Src, PKCdelta and Akt regulated protease activated receptor system in metastasis
    • 2011 - Cancer Council Queensland (Project Grant) - $200,000.00
      Funded ProjectA novel molecular pathway in cancer
    • 2010 - Wesley Research Institute (Project Grant) - $0.00
      Funded ProjectGenetic analysis of colorectal tumour initiating cells
    • 2010 - Prostate Cancer Foundation of Australia (Project Grant) - $0.00
      Funded ProjectNext generation DNA sequence analysis of prostate tumour initiating cells
    • 2009 - NHMRC (Project Grant) - $0.00
      Funded ProjectA novel receptor activated pathway in prostate cancer
    • 2009 - NHMRC (Project Grant) - $0.00
      Funded ProjectThe role of matriptase-2 and hemojuvelin in iron metabolism
    • 2009 - ARC (Equipment Grant) - $0.00
      Funded ProjectComprehensive cell imaging facility
    • 2004 - NHMRC (RD Wright Fellowship Career Development Award ) - $0.00
      Funded Project
    • 2000 - NHMRC (CJ Martin/RG Menzies Fellowship ) - $0.00
      Funded Project

    Publications

    MUC13 overexpression in renal cell carcinoma plays a central role in tumor progression and drug resistance
    2017 - Journal Article - DOI: 10.1002/ijc.30651
    Sheng, Yonghua, Ng, Choa Ping, Lourie, Rohan, Shah, Esha T., He, Yaowu, Wong, Kuan Yua, Seim, Inge, Oancea, Iulia, Morais, Christudas, Jeffery, Penny L., Hooper, John, Gobe, Glenda C. and Mcguckin, Michael A.

    Read Abstract

    Metastatic renal cell carcinoma is a largely incurable disease, and existing treatments targeting angiogenesis and tyrosine kinase receptors are only partially effective. Here we reveal that MUC13, a cell surface mucin glycoprotein, is aberrantly expressed by most renal cell carcinomas, with increasing expression positively correlating with tumor grade. Importantly, we demonstrated that high MUC13 expression was a statistically significant independent predictor of poor survival in two independent cohorts, particularly in stage 1 cancers. In cultured renal cell carcinoma cells MUC13 promoted proliferation and induced the cell cycle regulator, cyclin D1, and inhibited apoptosis by inducing the anti-apoptotic proteins, BCL-xL and survivin. Silencing of MUC13 expression inhibited migration and invasion, and sensitized renal cancer cells to killing by the multi-kinase inhibitors used clinically, sorafenib and sunitinib, and reversed acquired resistance to these drugs. Furthermore, we demonstrated that MUC13 promotion of renal cancer cell growth and survival is mediated by activation of nuclear factor κB, a transcription factor known to regulate the expression of genes that play key roles in the development and progression of cancer. These results show that MUC13 has potential as a prognostic marker for aggressive early stage renal cell cancer and is a plausible target to sensitize these tumors to therapy.


    Plasmin(ogen) serves as a favorable biomarker for prediction of survival in advanced high-grade serous ovarian cancer
    2017 - Journal Article - DOI: 10.1515/hsz-2016-0282
    Zhao, Shuo, Dorn, Julia, Napieralski, Rudolf, Walch, Axel, Diersch, Sandra, Kotzsch, Matthias, Ahmed, Nancy, Hooper, John D., Kiechle, Marion, Schmitt, Manfred and Magdolen, Viktor

    Read Abstract

    In serous ovarian cancer, the clinical relevance of tumor cell-expressed plasmin(ogen) (PLG) has not yet been evaluated. Due to its proteolytic activity, plasmin supports tumorigenesis, however, angiostatin(-like) fragments, derived from PLG, can also function as potent anti-tumorigenic factors. In the present study, we assessed PLG protein expression in 103 cases of advanced high-grade serous ovarian cancer (FIGO III/IV) by immunohistochemistry (IHC). In 70/103 cases, positive staining of tumor cells was observed. In univariate Cox regression analysis, PLG staining was positively associated with prolonged overall survival (OS) [hazard ratio (HR)=0.59, p=0.026] of the patients. In multivariable analysis, PLG, together with residual tumor mass, remained a statistically significant independent prognostic marker (HR=0.49, p=0.009). In another small patient cohort (n=29), we assessed mRNA expression levels of PLG by quantitative PCR. Here, elevated PLG mRNA levels were also significantly associated with prolonged OS of patients (Kaplan-Meier analysis; p=0.001). This finding was validated by in silico analysis of a microarray data set (n=398) from The Cancer Genome Atlas (Kaplan-Meier analysis; p=0.031). In summary, these data indicate that elevated PLG expression represents a favorable prognostic biomarker in advanced (FIGO III/IV) high-grade serous ovarian cancer.


    CD169+ macrophages mediate pathological formation of woven bone in skeletal lesions of prostate cancer
    2016 - Journal Article - DOI: 10.1002/path.4718
    Wu, Andy C., He, Yaowu, Broomfield, Amy, Paatan, Nicoll J., Harrington, Brittney S., Tseng, Hsu-Wen, Beaven, Elizabeth A., Kiernan, Deirdre M., Swindle, Peter, Clubb, Adrian B., Levesque, Jean-Pierre, Winkler, Ingrid G., Ling, Ming-Tat, Srinivasan, Bhuvana, Hooper, John D. and Pettit, Allison R.

    Read Abstract

    Skeletal metastases present a major clinical challenge for prostate cancer patient care, inflicting distinctive mixed osteoblastic and osteolytic lesions that cause morbidity and refractory skeletal complications. Macrophages are abundant in bone and bone marrow and can influence both osteoblast and osteoclast function in physiology and pathology. Herein we examined the role of macrophages in prostate cancer bone lesions, particularly the osteoblastic response. First, macrophage and lymphocyte distributions were qualitatively assessed in patient's prostate cancer skeletal lesions by immunohistochemistry. Second, macrophage functional contributions to prostate tumour growth in bone were explored using an immune-competent mouse model combined with two independent approaches to achieve in vivo macrophage depletion: liposome encapsulated clodronate that depletes phagocytic cells (including macrophages and osteoclasts); and targeted depletion of CD169+ macrophages using a suicide gene knock-in model. Immunohistochemistry and histomorphometric analysis were performed to quantitatively assess cancer-induced bone changes. In human bone metastasis specimens, CD68+ macrophages were consistently located within the tumour mass and at the tumour/bone marrow margins. Osteal macrophages (osteomacs) were associated with pathological woven bone within the metastatic lesions. In contrast, lymphocytes were inconsistently present in prostate cancer skeletal lesions and when detected had varied distributions. In the immune-competent mouse model, CD169+ macrophage ablation significantly inhibited prostate cancer-induced woven bone formation suggesting that CD169+ macrophages within pathological woven bone are integral to tumour-induced bone formation. In contrast pan-phagocytic, but not targeted CD169+ macrophage depletion resulted in increased tumour mass, indicating that CD169neg macrophage subset(s) and/or osteoclasts influenced tumour growth. In summary, these observations indicate a prominent role for macrophages in prostate cancer bone metastasis that may be therapeutically targetable to reduce the negative skeletal impacts of this malignancy, including tumour-induced bone modelling.


    Cell line and patient-derived xenograft models reveal elevated CDCP1 as a target in high-grade serous ovarian cancer
    2016 - Journal Article - DOI: 10.1038/bjc.2015.471
    Harrington, Brittney S., He, Yaowu, Davies, Claire M., Wallace, Sarah J., Adams, Mark N., Beaven, Elizabeth A., Roche, Deborah K., Kennedy, Catherine, Chetty, Naven P., Crandon, Alexander J., Flatley, Christopher, Oliveira, Niara B., Shannon, Catherine M., deFazio, Anna, Tinker, Anna V., Gilks, C. Blake, Gabrielli, Brian, Brennan, Donal J., Coward, Jermaine I., Armes, Jane E., Perrin, Lewis C. and Hooper, John D.

    Read Abstract

    Background: Development of targeted therapies for high-grade serous ovarian cancer (HGSC) remains challenging, as contributing molecular pathways are poorly defined or expressed heterogeneously. CUB-domain containing protein 1 (CDCP1) is a cell-surface protein elevated in lung, colorectal, pancreas, renal and clear cell ovarian cancer.

    Methods: CUB-domain containing protein 1 was examined by immunohistochemistry in HGSC and fallopian tube. The impact of targeting CDCP1 on cell growth and migration in vitro, and intraperitoneal xenograft growth in mice was examined. Three patient-derived xenograft (PDX) mouse models were developed and characterised for CDCP1 expression. The effect of a monoclonal anti-CDCP1 antibody on PDX growth was examined. Src activation was assessed by western blot analysis.

    Results: Elevated CDCP1 was observed in 77% of HGSC cases. Silencing of CDCP1 reduced migration and non-adherent cell growth in vitro and tumour burden in vivo. Expression of CDCP1 in patient samples was maintained in PDX models. Antibody blockade of CDCP1 significantly reduced growth of an HGSC PDX. The CDCP1-mediated activation of Src was observed in cultured cells and mouse xenografts.

    Conclusions: CUB-domain containing protein 1 is over-expressed by the majority of HGSCs. In vitro and mouse model data indicate that CDCP1 has a role in HGSC and that it can be targeted to inhibit progression of this cancer.


    Elevated CDCP1 predicts poor patient outcome and mediates ovarian clear cell carcinoma by promoting tumor spheroid formation, cell migration and chemoresistance
    2016 - Journal Article - DOI: 10.1038/onc.2015.101
    He, Y., Wu, A. C., Harrington, B. S., Davies, C. M., Wallace, S. J., Adams, M. N., Palmer, J. S., Roche, D. K., Hollier, B. G., Westbrook, T. F., Hamidi, H., Konecny, G. E., Winterhoff, B., Chetty, N. P., Crandon, A. J., Oliveira, N. B., Shannon, C. M., Tinker, A. V., Gilks, C. B., Coward, J. I., Lumley, J. W., Perrin, L. C., Armes, J. E. and Hooper, J. D.

    Read Abstract

    Hematogenous metastases are rarely present at diagnosis of ovarian clear cell carcinoma (OCC). Instead dissemination of these tumors is characteristically via direct extension of the primary tumor into nearby organs and the spread of exfoliated tumor cells throughout the peritoneum, initially via the peritoneal fluid, and later via ascites that accumulates as a result of disruption of the lymphatic system. The molecular mechanisms orchestrating these processes are uncertain. In particular, the signaling pathways used by malignant cells to survive the stresses of anchorage-free growth in peritoneal fluid and ascites, and to colonize remote sites, are poorly defined. We demonstrate that the transmembrane glycoprotein CUB-domain-containing protein 1 (CDCP1) has important and inhibitable roles in these processes. In vitro assays indicate that CDCP1 mediates formation and survival of OCC spheroids, as well as cell migration and chemoresistance. Disruption of CDCP1 via silencing and antibody-mediated inhibition markedly reduce the ability of TOV21G OCC cells to form intraperitoneal tumors and induce accumulation of ascites in mice. Mechanistically our data suggest that CDCP1 effects are mediated via a novel mechanism of protein kinase B (Akt) activation. Immunohistochemical analysis also suggested that CDCP1 is functionally important in OCC, with its expression elevated in 90% of 198 OCC tumors and increased CDCP1 expression correlating with poor patient disease-free and overall survival. This analysis also showed that CDCP1 is largely restricted to the surface of malignant cells where it is accessible to therapeutic antibodies. Importantly, antibody-mediated blockade of CDCP1 in vivo significantly increased the anti-tumor efficacy of carboplatin, the chemotherapy most commonly used to treat OCC. In summary, our data indicate that CDCP1 is important in the progression of OCC and that targeting pathways mediated by this protein may be useful for the management of OCC, potentially in combination with chemotherapies and agents targeting the Akt pathway.


    MUC13 protects colorectal cancer cells from death by activating the NF-κB pathway and is a potential therapeutic target
    2016 - Journal Article - DOI: 10.1038/onc.2016.241
    Sheng, Y. H., He, Y., Hasnain, S. Z., Wang, R., Tong, H., Clarke, D. T., Lourie, R., Oancea, I., Wong, K. Y., Lumley, J. W., Florin, T. H., Sutton, P., Hooper, J. D., McMillan, N. A. and McGuckin, M. A.

    Read Abstract

    MUC13 is a transmembrane mucin glycoprotein that is over produced by many cancers, although its functions are not fully understood. Nuclear factor-κB (NF-κB) is a key transcription factor promoting cancer cell survival, but therapeutically targeting this pathway has proved difficult because NF-κB has pleiotropic functions. Here, we report that MUC13 prevents colorectal cancer cell death by promoting two distinct pathways of NF-kB activation, consequently upregulating BCL-XL. MUC13 promoted tumor necrosis factor (TNF)-induced NF-κB activation by interacting with TNFR1 and the E3 ligase, cIAP1, to increase ubiquitination of RIPK1. MUC13 also promoted genotoxin-induced NF-κB activation by increasing phosphorylation of ATM and SUMOylation of NF-κB essential modulator. Moreover, elevated expression of cytoplasmic MUC13 and NF-κB correlated with colorectal cancer progression and metastases. Our demonstration that MUC13 enhances NF-κB signaling in response to both TNF and DNA-damaging agents provides a new molecular target for specific inhibition of NF-κB activation. As proof of principle, silencing MUC13 sensitized colorectal cancer cells to killing by cytotoxic drugs and inflammatory signals and abolished chemotherapy-induced enrichment of CD133+ CD44+ cancer stem cells, slowed xenograft growth in mice, and synergized with 5-fluourouracil to induce tumor regression. Therefore, these data indicate that combining chemotherapy and MUC13 antagonism could improve the treatment of metastatic cancers.


    New crossroads for potential therapeutic intervention in cancer - intersections between CDCP1, EGFR family members and downstream signaling pathways
    2016 - Journal Article - DOI: 10.18632/oncoscience.286
    He, Yaowu, Harrington, Brittney S. and Hooper, John D.

    Read Abstract

    Signaling pathways regulated by the receptor CDCP1 play central roles in promoting cancer and in mediating resistance to chemo- and targeted-therapies. In this perspective we briefly summarize these findings as well as data demonstrating poorer outcomes for several malignancies that exhibit elevated CDCP1 expression. Promising data from preclinical studies suggest that CDCP1 targeted agents, including therapeutic antibodies, could be useful in the treatment of cancer patients selected on the basis of activation of CDCP1 and its signaling partners including EGFR, HER2, Met and Src.


    Potent small agonists of protease activated receptor 2
    2016 - Journal Article - DOI: 10.1021/acsmedchemlett.5b00429
    Yau, Mei-Kwan, Suen, Jacky Y., Xu, Weijun, Lim, Junxian, Liu, Ligong, Adams, Mark N., He, Yaowu, Hooper, John D., Reid, Robert C. and Fairlie, David P.

    Read Abstract

    Many proteases cut the PAR2 N-terminus resulting in conformational changes that activate cells. Synthetic peptides corresponding to newly exposed N-terminal sequences of PAR2 also activate the receptor at micromolar concentrations. PAR2-selective small molecules reported here induce PAR2-mediated intracellular calcium signaling at nanomolar concentrations (EC50 = 15–100 nM, iCa2+, CHO-hPAR2 cells). These are the most potent and efficient small molecule ligands to activate PAR2-mediated calcium release and chemotaxis, including for human breast and prostate cancer cells.


    A critical role for murine transferrin receptor 2 in erythropoiesis during iron restriction
    2015 - Journal Article - DOI: 10.1111/bjh.13225
    Wallace, Daniel F., Secondes, Eriza S., Rishi, Gautam, Ostini, Lesa, McDonald, Cameron J., Lane, Steven W., Vu, Therese, Hooper, John D., Velasco, Gloria, Ramsay, Andrew J., Lopez-Otin, Carlos and Subramaniam, V. Nathan

    Read Abstract

    Effective erythropoiesis requires an appropriate supply of iron and mechanisms regulating iron homeostasis and erythropoiesis are intrinsically linked. Iron dysregulation, typified by iron-deficiency anaemia and iron overload, is common in many clinical conditions and impacts the health of up to 30% of the world's population. The proteins transmembrane protease, serine 6 (TMPRSS6; also termed matriptase-2), HFE and transferrin receptor 2 (TFR2) play important and opposing roles in systemic iron homeostasis, by regulating expression of the iron regulatory hormone hepcidin. We have performed a systematic analysis of mice deficient in these three proteins and show that TMPRSS6 predominates over HFE and TFR2 in hepcidin regulation. The phenotype of mice lacking TMPRSS6 and TFR2 is characterized by severe anaemia and extramedullary haematopoiesis in the spleen. Stress erythropoiesis in these mice results in increased expression of the newly identified erythroid iron regulator erythroferrone, which does not appear to overcome the hepcidin overproduction mediated by loss of TMPRSS6. Extended analysis reveals that TFR2 plays an important role in erythroid cells, where it is involved in terminal erythroblast differentiation and the regulation of erythropoietin. In conclusion, we have identified an essential role for TFR2 in erythropoiesis that may provide new targets for the treatment of anaemia.


    Cancer stem cell markers in prostate cancer: An immunohistochemical study of ALDH1, SOX2 and EZH2
    2015 - Journal Article - DOI: 10.1097/pat.0000000000000325
    Matsika, Admire, Srinivasan, Bhuvana, Day, Christopher, Mader, Sabina Ann, Kiernan, Deirdre Margaret, Broomfield, Amy, Fu, Jinlin, Hooper, John D., Kench, James G. and Samaratunga, Hemamali

    Read Abstract

    Summary:  The aims of this study were to investigate the immunohistochemical expression and potential prognostic significance of putative cancer stems cell markers ALDH1, EZH2 and SOX2 in prostate cancer.
    A total of 142 consecutive radical prostatectomies submitted to one laboratory with a diagnosis of prostatic adenocarcinoma between 2008 and 2012 were retrieved and retrospectively studied. Immunohistochemistry for the three markers was performed in each case and both univariate and multivariate analyses were undertaken to evaluate the correlation between the staining patterns and known histopathological prognostic features.
    ALDH1 showed a statistically significant association with tumour stage p < 0.001), extraprostatic extension (p < 0.001) and lymphovascular invasion (p = 0.001). EZH2 correlated with Gleason score (p = 0.044) and lymph node metastases (p = 0.023). SOX2 showed a statistically significant correlation with lymphovascular invasion only (p = 0.018) in both univariate and multivariate analyses.
    Cancer stem cell markers are variably expressed in prostate adenocarcinoma and immunohistochemical staining for ALDH1 and EZH2 may have a role in predicting tumour aggressiveness before treatment of prostate cancer.

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    Awards

    • Sr Regis Mary Dunne Medal for outstanding research contribution
      Awarding Body: Mater Medical Research Institute
      Year awarded: 2011

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