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Oncogenesis 7건

  1. [해외논문]   Grainyhead-like 2 (GRHL2) knockout abolishes oral cancer development through reciprocal regulation of the MAP kinase and TGF-β signaling pathways   SCIE

    Chen, Wei (The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA USA ) , Kang, Kyung L. (The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA USA ) , Alshaikh, Abdullah (The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA USA ) , Varma, Saaket (The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA USA ) , Lin, Yi-Ling (Division of Diagnostic and Surgical Sciences, UCLA School of Dentistry, Los Angeles, CA USA ) , Shin, Ki-Hyuk (The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA USA ) , Kim, Reuben (The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA USA ) , Wang, Cun-Yu (Division of Oral Biology and Medicine, UCLA School of Dentistry, Los Angeles, USA ) , Park, No-Hee (The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA USA ) , Walentin, Katharina (Max Delbru) , Schmidt-Ott, Kai M. , Kang, Mo K.
    Oncogenesis v.7 no.5 ,pp. 38 , 2018 ,

    초록

    Grainyhead-Like 2 (GRHL2) is an epithelial-specific transcription factor that regulates epithelial morphogenesis and differentiation. Prior studies suggested inverse regulation between GRHL2 and TGF-β in epithelial plasticity and potential carcinogenesis. Here, we report the role of GRHL2 in oral carcinogenesis in vivo using a novel Grhl2 knockout (KO) mouse model and the underlying mechanism involving its functional interaction with TGF-β signaling. We developed epithelial-specific Grhl2 conditional KO mice by crossing Grhl2 floxed mice with those expressing CreER driven by the K14 promoter. After induction of Grhl2 KO, we confirmed the loss of GRHL2 and its target proteins, while Grhl2 KO strongly induced TGF-β signaling molecules. When exposed to 4-nitroquinoline 1-oxide (4-NQO), a strong chemical carcinogen, Grhl2 wild-type (WT) mice developed rampant oral tongue tumors, while Grhl2 KO mice completely abolished tumor development. In cultured oral squamous cell carcinoma (OSCC) cell lines, TGF-β signaling was notably induced by GRHL2 knockdown while being suppressed by GRHL2 overexpression. GRHL2 knockdown or KO in vitro and in vivo, respectively, led to loss of active p-Erk1/2 and p-JNK MAP kinase levels; moreover, ectopic overexpression of GRHL2 strongly induced the MAP kinase activation. Furthermore, the suppressive effect of GRHL2 on TGF-β signaling was diminished in cells exposed to Erk and JNK inhibitors. These data indicate that GRHL2 activates the Erk and JNK MAP kinases, which in turn suppresses the TGF -β signaling. This novel signaling represents an alternative pathway by which GRHL2 regulates carcinogenesis, and is distinct from the direct transcriptional regulation by GRHL2 binding at its target gene promoters, e.g., E-cadherin, hTERT, p63, and miR-200 family genes. Taken together, the current study provides the first genetic evidence to support the role of GRHL2 in carcinogenesis and the underlying novel mechanism that involves the functional interaction between GRHL2 and TGF-β signaling through the MAPK pathways.

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  2. [해외논문]   CARF enrichment promotes epithelial–mesenchymal transition via Wnt/β-catenin signaling: its clinical relevance and potential as a therapeutic target   SCIE

    Kalra, Rajkumar S. (Drug Discovery and Assets Innovation Lab, DBT-AIST International Laboratory for Advanced Biomedicine (DAILAB), DAICENTER, National Institute of Advanced Industrial Science & Technology (AIST), Tsukuba, Ibaraki, 305-8565, Japan ) , Chaudhary, Anupama (Drug Discovery and Assets Innovation Lab, DBT-AIST International Laboratory for Advanced Biomedicine (DAILAB), DAICENTER, National Institute of Advanced Industrial Science & Technology (AIST), Tsukuba, Ibaraki, 305-8565, Japan ) , Yoon, A-Rum (Department of Bioengineering, College of Engineering, Hanyang University, Seongdong-gu, Seoul, Korea ) , Bhargava, Priyanshu (Drug Discovery and Assets Innovation Lab, DBT-AIST International Laboratory for Advanced Biomedicine (DAILAB), DAICENTER, National Institute of Advanced Industrial Science & Technology (AIST), Tsukuba, Ibaraki, 305-8565, Japan ) , Omar, Amr (Drug Discovery and Assets Innovation Lab, DBT-AIST International Laboratory for Advanced Biomedicine (DAILAB), DAICENTER, National Institute of Advanced Industrial Science & Technology (AIST), Tsukuba, Ibaraki,) , Garg, Sukant , Yun, Chae-Ok , Kaul, Sunil C. , Wadhwa, Renu
    Oncogenesis v.7 no.5 ,pp. 39 - 39 , 2018 ,

    초록

    CARF (Collaborator of ARF)/CDKN2AIP was discovered as a novel ARF-binding protein. It has been established as an essential cell survival, p53-, and cell proliferation-regulatory protein. Although a moderate upregulation of CARF caused growth arrest and senescence, its excessively enriched levels were shown to facilitate aggressive proliferation and malignant transformation of cancer cells. Here, we examined the relevance of CARF levels in clinical tumors and found its amplification (both at gene and transcript levels) in a variety of invasive and metastatic malignancies. Consistent with the clinical readouts, enrichment of CARF in cancer cells promoted epithelial-mesenchymal transition (EMT). Cancer database and molecular analyses revealed that it activates Wnt/beta-catenin signaling axis, as evident by enhanced nuclear localization and function of 13-catenin marked by increased level of SNAIL1, SNAIL2, ZEB1, and TWIST1 and its downstream gene targets. Of note, targeted knockdown of CARF led to decrease in nuclear beta-catenin and its key downstream effectors, involved in EMT progression. Consistent with this, CARF targeting in vivo either by naked siRNA or CARF shRNA harboring adeno-oncolytic virus caused suppression of tumor progression and lung metastasis. Taken together, we report clinical and therapeutic relevance of CARF in EMT and cancer invasiveness/metastasis, and propose it as a potent therapeutic target of aggressive cancers.

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  3. [해외논문]   Dysregulation of the MiR-449b target TGFBI alters the TGFβ pathway to induce cisplatin resistance in nasopharyngeal carcinoma   SCIE

    Bissey, Pierre-Antoine (Princess Margaret Cancer Centre, University Health Network, Toronto, ON Canada ) , Law, Jacqueline H. (Department of Medical Biophysics, University of Toronto, Toronto, ON Canada ) , Bruce, Jeff P. (Princess Margaret Cancer Centre, University Health Network, Toronto, ON Canada ) , Shi, Wei (Princess Margaret Cancer Centre, University Health Network, Toronto, ON Canada ) , Renoult, Aline (LabEx DEVweCAN, Université) , Chua, Melvin L. K. (de Lyon, F-69000 Lyon, France ) , Yip, Kenneth W. (Princess Margaret Cancer Centre, University Health Network, Toronto, ON Canada ) , Liu, Fei-Fei (Princess Margaret Cancer Centre, University Health Network, Toronto, ON Canada )
    Oncogenesis v.7 no.5 ,pp. 40 , 2018 ,

    초록

    Despite the improvement in locoregional control of nasopharyngeal carcinoma (NPC), distant metastasis (DM), and chemoresistance persist as major causes of mortality. This study identified a novel role for miR-449b, an overexpressed gene in a validated four-miRNA signature for NPC DM, leading to chemoresistance via the direct targeting of transforming growth factor beta-induced (TGFBI). In vitro shRNA-mediated downregulation of TGFBI induced phosphorylation of PTEN and AKT, increasing cisplatin resistance. Conversely, the overexpression of TGFBI sensitized the NPC cells to cisplatin. In NPC patients treated with concurrent chemoradiotherapy (CRT), the overall survival (OS) was significantly inversely correlated with miR-449b, and directly correlated with both TGFBI mRNA and protein expression, as assessed by RNA sequencing and immunohistochemistry (IHC). Mechanistically, co-immunoprecipitation demonstrated that TGFBI competes with pro-TGFβ1 for integrin receptor binding. Decreased TGFBI led to increased pro-TGFβ1 activation and TGFβ1 canonical/noncanonical pathway-induced cisplatin resistance. Thus, overexpression of miR-449b decreases TGFBI, thereby altering the balance between TGFBI and pro-TGFβ1, revealing a novel mechanism of chemoresistance in NPC.

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  4. [해외논문]   Tumor-derived exosomes induce PD1 + macrophage population in human gastric cancer that promotes disease progression   SCIE

    Wang, Furong (Department of Pathology, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, Lanzhou, China ) , Li, Bin (Department of Thoracic Surgery, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, Lanzhou, China ) , Wei, Yucai (School of Basic Medical Science, Lanzhou University, Lanzhou, 730000 China ) , Zhao, Yang (Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, Lanzhou, China ) , Wang, Li (School of Basic Medical Science, Lanzhou University, Lanzhou, 730000 China ) , Zhang, Peng (Department of Pathology, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, Lanzhou, China ) , Yang, Jinwei (Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Second Clinical Medical College, Lanzhou, China ) , He, Wenting (Gansu Provincial Key Laboratory of Digestive System Tumors, Lanzhou University Second Hospital, Lanzhou University Seco) , Chen, Hao , Jiao, Zuoyi , Li, Yumin
    Oncogenesis v.7 no.5 ,pp. 41 , 2018 ,

    초록

    Macrophages constitute a major component of tumor-infiltrating immune cells. M2 macrophages have been reported to promote tumor progression through promoting tumor angiogenesis and metastasis and regulating T-cell function. Here, we identified a protumorigenic subset of macrophages that constitutively expressed programmed cell death 1 (PD1) and accumulated in advanced-stage gastric cancer (GC). These PD1 + tumor-associated macrophages (TAMs) exhibited an M2-like surface profile, with a significant increase in the expression of CD206, IL-10, and CCL1, and a clear decrease in the expression of MHC class II, CD64, and IL-12 and the ability to phagocytose ovalbumin. Moreover, PD1 + TAMs can suppress CD8 + T-cell function and this immunosuppressive activity can effectively be enhanced upon triggering PD1 signal. GC-derived exosomes effectively educated monocytes to differentiate into PD1 + TAMs with M2 phenotypic and functional characteristics. Together, our results are the first to show that GC-derived exosomes can effectively induce PD1 + TAM generation, and these cells can produce a large number of IL-10, impair CD8 + T-cell function, and thereby create conditions that promote GC progression. Thus, methods in which immunotherapy is combined with targeting PD1 + TAMs and tumor-derived exosomes should be used to restore immune function in GC patients.

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  5. [해외논문]   NOTCH3 inactivation increases triple negative breast cancer sensitivity to gefitinib by promoting EGFR tyrosine dephosphorylation and its intracellular arrest   SCIE

    Diluvio, Giulia (Department of Molecular Medicine, Sapienza University, Rome, Italy ) , Del Gaudio, Francesca (Department of Cell and Molecular Biology, Karolinska Institutet, 17177, Stockolm, Sweden ) , Giuli, Maria Valeria (Department of Molecular Medicine, Sapienza University, Rome, Italy ) , Franciosa, Giulia (Novo Nordisk Foundation Center for Protein Research, University of Cophenagen, København, Denmark ) , Giuliani, Eugenia (Department of Molecular Medicine, Sapienza University, Rome, Italy ) , Palermo, Rocco (Department of Molecular Medicine, Sapienza University, Rome, Italy ) , Besharat, Zein Mersini (Center for Life Nano Science@Sapienza, Istituto Italiano di Tecnologia, Rome, Italy ) , Pignataro, Maria Gemma (Department of Molecular Medicine, Sapienza University, Rome, Italy ) , Vacca, Alessandra (Department of Radiological, Oncological and Pathological Sciences, Sapienza University, Rome, Italy ) , d'Amati, Giulia (Department of Experimental Medicine, Sapienza University, Rome, Italy ) , Maroder, Marella (Department of Radiological, Oncological and Pathological Sciences, Sapienza University, Rome, Italy ) , Talora, Claudio (Department of Medico-Surgical Sciences and Biotechnology, Sapienza University, Latina, Italy ) , Capalbo, Carlo (Depar) , Bellavia, Diana , Checquolo, Saula
    Oncogenesis v.7 no.5 ,pp. 42 - 42 , 2018 ,

    초록

    Notch dysregulation has been implicated in numerous tumors, including triple-negative breast cancer (TNBC), which is the breast cancer subtype with the worst clinical outcome. However, the importance of individual receptors in TNBC and their specific mechanism of action remain to be elucidated, even if recent findings suggested a specific role of activated-Notch3 in a subset of TNBCs. Epidermal growth factor receptor (EGFR) is overexpressed in TNBCs but the use of anti-EGFR agents (including tyrosine kinase inhibitors, TKIs) has not been approved for the treatment of these patients, as clinical trials have shown disappointing results. Resistance to EGFR blockers is commonly reported. Here we show that Notch3-specific inhibition increases TNBC sensitivity to the TKI-gefitinib in TNBC-resistant cells. Mechanistically, we demonstrate that Notch3 is able to regulate the activated EGFR membrane localization into lipid rafts microdomains, as Notch3 inhibition, such as rafts depletion, induces the EGFR internalization and its intracellular arrest, without involving receptor degradation. Interestingly, these events are associated with the EGFR tyrosine dephosphorylation at Y1173 residue (but not at Y1068) by the protein tyrosine phosphatase H1 (PTPH1), thus suggesting its possible involvement in the observed Notch3-dependent TNBC sensitivity response to gefitinib. Consistent with this notion, a nuclear localization defect of phospho-EGFR is observed after combined blockade of EGFR and Notch3, which results in a decreased TNBC cell survival. Notably, we observed a significant correlation between EGFR and NOTCH3 expression levels by in silico gene expression and immunohistochemical analysis of human TNBC primary samples. Our findings strongly suggest that combined therapies of TKI-gefitinib with Notch3-specific suppression may be exploited as a drug combination advantage in TNBC treatment.

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  6. [해외논문]   AIRE promotes androgen-independent prostate cancer by directly regulating IL-6 and modulating tumor microenvironment   SCIE

    Kalra, Rashi (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India ) , Bhagyaraj, Ella (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India ) , Tiwari, Drishti (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India ) , Nanduri, Ravikanth (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India ) , Chacko, Anuja P. (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India ) , Jain, Monika (Department of Molecular Biology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India ) , Mahajan, Sahil (Department of Molecular Biology, Council of Scientific and Industrial) , Khatri, Neeraj , Gupta, Pawan
    Oncogenesis v.7 no.5 ,pp. 43 - 43 , 2018 ,

    초록

    Early stage prostate cancers are dependent on androgens for their growth and survival and androgen withdrawal causes them to regress. Progressive prostate cancers eventually acquire androgen independence rendering anti-androgen therapy ineffective. However, the factors leading to this have not been adequately addressed. This study shows that AIRE finds differential expression in androgen-dependent and -independent prostate cancer cells. AIRE expression is more in androgen-independent cells due to its regulation by transcription factor Elk-1. These enhanced levels of AIRE modulate the prostate tumor microenvironment by transcriptionally activating a malignancy gene IL-6 in androgen-independent cells. Additionally, AIRE prevents the cancer cells from anticancer drug-induced death and enhances their invasiveness. Moreover, AIRE by modulating the cytokine milieu skews the tumor-associated macrophage polarization towards M2 phenotype with increased CD206 and CD163 expression. Subcutaneous mouse model of prostate cancer revealed AIRE +/+ mice forming a palpable tumor and presents lymphadenopathy however, only a small benign tumor is observed in AIRE −/− mice and lymph nodes appear normal in size. In conclusion, our findings suggest AIRE as a probable factor in promoting prostate cancer progression.

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  7. [해외논문]   Hepatitis transactivator protein X promotes extracellular matrix modification through HIF/LOX pathway in liver cancer   SCIE

    Tse, Aki Pui-Wah (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Sze, Karen Man-Fong (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Shea, Queenie Tsung-Kwan (Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong, China ) , Chiu, Elley Yung-Tuen (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Tsang, Felice Ho-Ching (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Chiu, David Kung-Chun (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Zhang, Misty Shuo (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Lee, Derek (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Xu, Iris Ming-Jing (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Chan, Cerise Yuen-Ki (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Koh, Hui-Yu (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Wong, Chun-Ming (Department of Pathology, The University of Hong Kong, Hong Kong, China ) , Zheng, Yong-Ping (Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong, China ) , Ng, Irene Oi-Lin (Departm) , Wong, Carmen Chak-Lui
    Oncogenesis v.7 no.5 ,pp. 44 , 2018 ,

    초록

    Hepatocellular carcinoma (HCC), accounting for 90% of primary liver cancer, is a lethal malignancy that is tightly associated with chronic hepatitis B virus (HBV) infection. HBV encodes a viral onco-protein, transactivator protein X (HBx), which interacts with proteins of hepatocytes to promote oncogenesis. Our current study focused on the interaction of HBx with a transcription factor, hypoxia-inducible factor-1α (HIF-1α), which is stabilized by low O 2 condition (hypoxia) and is found to be frequently overexpressed in HCC intra-tumorally due to poor blood perfusion. Here, we showed that overexpression of HBx by tetracycline-inducible systems further stabilized HIF-1α under hypoxia in HBV-negative HCC cell lines. Reversely, knockdown of HBx reduced HIF-1α protein stabilization under hypoxia in HBV-positive HCC cell lines. More intriguingly, overexpression of HBx elevated the mRNA and protein expression of a family of HIF-1α target genes, the lysyl oxidase (LOX) family in HCC. The LOX family members function to cross-link collagen in the extracellular matrix (ECM) to promote cancer progression and metastasis. By analyzing the collagens under scanning electron microscope, we found that collagen fibers were significantly smaller in size when incubated with conditioned medium from HBx knockdown HCC cells as compared to control HCC cells in vitro. Transwell invasion assay further revealed that less cells were able to invade through the matrigel which was pre-treated with conditioned medium from HBx knockdown HCC cells as compared to control HCC cells. Orthotopic and subcutaneous HCC models further showed that knockdown of HBx in HCC cells reduced collagen crosslinking and stiffness in vivo and repressed HCC growth and metastasis. Taken together, our in vitro and in vivo studies showed the HBx remodeled the ECM through HIF-1α/LOX pathway to promote HCC metastasis.

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