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  • 1
    Online Resource
    Online Resource
    LC3A-mediated autophagy regulates lung cancer cell plasticity
    Informa UK Limited ; 2022
    In:  Autophagy Vol. 18, No. 4 ( 2022-04-03), p. 921-934
    Details
    In: Autophagy, Informa UK Limited, Vol. 18, No. 4 ( 2022-04-03), p. 921-934
    Type of Medium: Online Resource
    ISSN: 1554-8627 , 1554-8635
    URL: Article
    DOI: 10.1080/15548627.2021.1964224
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2022
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  • 2
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    Correction: Periostin promotes ovarian cancer metastasis by enhancing M2 macrophages and cancer-associated fibroblasts via integrin-mediated NF-κB and TGF-β2 signaling
    Springer Science and Business Media LLC ; 2023
    In:  Journal of Biomedical Science Vol. 30, No. 1 ( 2023-07-12)
    Details
    In: Journal of Biomedical Science, Springer Science and Business Media LLC, Vol. 30, No. 1 ( 2023-07-12)
    Type of Medium: Online Resource
    ISSN: 1423-0127
    URL: Article
    DOI: 10.1186/s12929-023-00948-w
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 1482918-6
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  • 3
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    Periostin promotes ovarian cancer metastasis by enhancing M2 macrophages and cancer-associated fibroblasts via integrin-mediated NF-κB and TGF-β2 signaling
    Springer Science and Business Media LLC ; 2022
    In:  Journal of Biomedical Science Vol. 29, No. 1 ( 2022-12-22)
    Details
    In: Journal of Biomedical Science, Springer Science and Business Media LLC, Vol. 29, No. 1 ( 2022-12-22)
    Abstract: Ovarian cancer has the highest mortality among gynecological cancers due to late diagnosis and lack of effective targeted therapy. Although the study of interplay between cancer cells with their microenvironment is emerging, how ovarian cancer triggers signaling that coordinates with immune cells to promote metastasis is still elusive. Methods Microarray and bioinformatics analysis of low and highly invasive ovarian cancer cell lines were used to reveal periostin (POSTN), a matrix protein with multifunctions in cancer, with elevated expression in the highly invasive cells. Anchorage independent assay, Western blot, RNA interference, confocal analysis and neutralizing antibody treatment were performed to analyze the effects of POSTN on tumor promotion and to explore the underlying mechanism. Chemotaxis, flow cytometry and cytokine array analyses were undertaken to analyze the involvement of POSTN in cancer-associated fibroblast (CAF) and macrophage modulation. Correlations between POSTN expression levels and clinical characteristics were analyzed using the Oncomine, commercial ovarian cancer cDNA and China Medical University Hospital patient cohort. In vivo effect of POSTN on metastasis was studied using a mouse xenograft model. Results Expression of POSTN was found to be elevated in highly invasive ovarian cancer cells. We observed that POSTN was co-localized with integrin β3 and integrin β5, which was important for POSTN-mediated activation of ERK and NF-κB. Ectopic expression of POSTN enhanced whereas knockdown of POSTN decreased cancer cell migration and invasion in vitro, as well as tumor growth and metastasis in vivo. POSTN enhanced integrin/ERK/NF-κB signaling through an autocrine effect on cancer cells to produce macrophage attracting and mobilizing cytokines including MIP-1β, MCP-1, TNFα and RANTES resulting in increased chemotaxis of THP-1 monocytes and their polarization to M2 macrophages in vitro. In agreement, tumors derived from POSTN-overexpressing SKOV3 harbored more tumor-associated macrophages than the control tumors. POSTN induced TGF-β2 expression from ovarian cancer cells to promote activation of adipose-derived stromal cells to become CAF-like cells expressing alpha smooth muscle actin and fibroblast activation protein alpha. Consistently, increased CAFs were observed in POSTN overexpressing SKOV3 cells-derived metastatic tumors. In clinical relevance, we found that expression of POSTN was positively correlated with advanced-stage diseases and poor overall survival of patients. Conclusions Our study revealed a POSTN-integrin-NF-κB-mediated signaling and its involvement in enhancing M2 macrophages and CAFs, which could potentially participate in promoting tumor growth. Our results suggest that POSTN could be a useful prognosis marker and potential therapeutic target.
    Type of Medium: Online Resource
    ISSN: 1423-0127
    URL: Article
    DOI: 10.1186/s12929-022-00888-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 1482918-6
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  • 4
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    Detrimental and Beneficial Effect of Autophagy and a Potential Therapeutic Target after Ischemic Stroke
    Hindawi Limited ; 2020
    In:  Evidence-Based Complementary and Alternative Medicine Vol. 2020 ( 2020-09-23), p. 1-10
    Details
    In: Evidence-Based Complementary and Alternative Medicine, Hindawi Limited, Vol. 2020 ( 2020-09-23), p. 1-10
    Abstract: Autophagy, a physiologic mechanism that promotes energy recycling and orderly degradation through self-regulated disassembly of cellular components, helps maintain homeostasis. A series of evidences suggest that autophagy is activated as a response to ischemia and has been well-characterized as a therapeutic target. However, the role of autophagy after ischemia remains controversial. Activated-autophagy can remove necrotic substances against ischemic injury to promote cell survival. On the contrary, activation of autophagy may further aggravate ischemic injury, causing cell death. Therefore, the present review will examine the current understanding of the precise mechanism and role of autophagy in ischemia and recent neuroprotective therapies on autophagy, drug therapies, and nondrug therapies, including electroacupuncture (EA).
    Type of Medium: Online Resource
    ISSN: 1741-4288 , 1741-427X
    URL: Article
    DOI: 10.1155/2020/8372647
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2148302-4
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  • 5
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    Abstract 2001: Krupple like factor 10 modulates stem cell phenotype of pancreatic adenocarcinoma via transcriptional regulation of Notch signal pathway
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Research Vol. 81, No. 13_Supplement ( 2021-07-01), p. 2001-2001
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 13_Supplement ( 2021-07-01), p. 2001-2001
    Abstract: Background: Pancreatic adenocarcinoma (PDAC) is known for its deregulated TGFβ signal pathway. Therapeutic strategy targeting TGFβ is controversial due to the dual role of TGFβ with anti-proliferation in early phase and pro-metastatic in late phase of cancer progression. KLF10, an early response gene of TGFβ, positively feedback the antiproliferative effect in cancer. Recent studies revealed KLF10 expression were suppressed epigenetically in various cancers including PDAC. In contrary to TGFβ, KLF10 transcriptionally suppress Slug and Sirtuin 6 to prevent metastasis in advanced PDAC. The role of KLF10 in regulating tumorigenesis and stem cell phenotype is still unknown. Materials and Methods: From 105 patients of resectable PDAC, KLF10 expression level was evaluated to be reduced in 62% of tumor specimens. Low KLF10 expression correlated with larger tumor size and rapid loco-regional recurrence. In murine model of Kras mutation (KC mice), additional depletion of KLF10 induced 57% of PDAC compared to 0% at 18 to 24 wk of age. PDAC cells were genetically manipulated with KLF10mRNA silencing (PDACshKLF10) or inducible overexpression (PDACoeKLF10). Using limiting dilution assay of tumor growth, and orthotopic tumor implantation, we found higher tumorigenic ability of PDACshKlf10 compared to that of wild type. The stem cell phenotypes of PDACshKLF10 and PDACoeKLF10 were confirmed by sphere formation assay and FACS analysis of surface markers including CD24/CD44, ESA/c-Met, CD47 and CD133. Results: Notch signal pathway was found to be significantly enhanced from microarray analysis of wild type versus PDACshKLF10 cells. The increased Notch signal molecules were confirmed in RNA and protein level in genetically manipulated PDAC cells as well as clinical tissue specimens. Using Chip-PCR and luciferase promoter assay, KLF10 was demonstrated to bind to the promoter of Notch receptor 1, 3, and 4. DAPT (N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester), a Notch inhibitor, suppressed in vitro spheroid formation, cell surface expression of stem cell markers, and tumor growth of PDACshKLF10 in orthotopic murine model. We conclude that KLF10 modulates stem cell phenotype of PDAC by transcriptionally suppressing Notch signal pathway. Loss of KLF10 in PDAC patients leads to Notch signal activation, development of stem cell phenotype and tumor progression. Notch inhibition may reverse malignant growth of PDAC with reduced KLF10 expression. Conflict of interest statement: nothing to declare Citation Format: Yi-Chih Tsai, Su-Liang Chen, Shu-Ling Peng, Kuang-Hung Cheng, Shih-Sheng Jiang, Shuang-En Chuang, Ch'ang Hui-Ju. Krupple like factor 10 modulates stem cell phenotype of pancreatic adenocarcinoma via transcriptional regulation of Notch signal pathway [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2001.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2021-2001
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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    detail.hit.zdb_id: 410466-3
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  • 6
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    Astragalus Polysaccharide (PG2) Suppresses Macrophage Migration Inhibitory Factor and Aggressiveness of Lung Adenocarcinoma Cells
    World Scientific Pub Co Pte Ltd ; 2020
    In:  The American Journal of Chinese Medicine Vol. 48, No. 06 ( 2020-01), p. 1491-1509
    Details
    In: The American Journal of Chinese Medicine, World Scientific Pub Co Pte Ltd, Vol. 48, No. 06 ( 2020-01), p. 1491-1509
    Abstract: Astragalus membranaceus is the most popular traditional Chinese medicine for managing vital energy deficiency. Its injectable polysaccharide PG2 has been used for relieving cancer-related fatigue, and PG2 has immune-modulatory and anti-inflammatory effects. In this study, we explored the effects of PG2 in lung adenocarcinoma A549 and CL1-2 cells and investigated its anticancer activity, and the results were validated in severe combined immunodeficiency (SCID) mice. Although PG2 did not inhibit the growth of these cells, it dose-dependently suppressed their migration and invasion, accompanied by reduced vimentin and AXL and induced epithelial cadherin (E-cadherin) expression. Regarding the underlying molecular mechanism, PG2 treatment reduced the macrophage migration inhibitory factor (MIF), an inflammatory cytokine that promotes the epithelial–mesenchymal transition and aggressiveness of cancer cells. Consistent with the previous finding that MIF regulates matrix metalloproteinase-13 (MMP-13) and AMP-activated protein kinase (AMPK), treatment with PG2 reduced MMP-13 and activated AMPK in A549 and CL1-2 cells in this study. In SCID mice injected with A549 cells through the tail vein, intraperitoneal injection with PG2 reduced lung and abdominal metastases in parallel with decreased immunohistochemical staining of AXL, vimentin, MMP-13, and MIF in the tumor. Collectively, data revealed a potential application of PG2 in integrative cancer treatment through the suppression of MIF in cancer cells and their aggressiveness.
    Type of Medium: Online Resource
    ISSN: 0192-415X , 1793-6853
    URL: Article
    DOI: 10.1142/S0192415X20500731
    Language: English
    Publisher: World Scientific Pub Co Pte Ltd
    Publication Date: 2020
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  • 7
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    Omega-3 Fatty Acid-Enriched Fish Oil and Selenium Combination Modulates Endoplasmic Reticulum Stress Response Elements and Reverses Acquired Gefitinib Resistance in HCC827 Lung Adenocarcinoma Cells
    MDPI AG ; 2020
    In:  Marine Drugs Vol. 18, No. 8 ( 2020-07-29), p. 399-
    Details
    In: Marine Drugs, MDPI AG, Vol. 18, No. 8 ( 2020-07-29), p. 399-
    Abstract: Non-small cell lung cancer (NSCLC)-carrying specific epidermal growth factor receptor (EGFR) mutations can be effectively treated by a tyrosine kinase inhibitor such as gefitinib. However, the inevitable development of acquired resistance leads to the eventual failure of therapy. In this study, we show the combination effect of omega-3 fatty acid-enriched fish oil (FO) and selenium (Se) on reversing the acquired gefitinib-resistance of HCC827 NSCLC cells. The gefitinib-resistant subline HCC827GR possesses lowered proapoptotic CHOP (CCAAT/enhancer-binding protein homologous protein) and elevated cytoprotective GRP78 (glucose regulated protein of a 78 kDa molecular weight) endoplasmic reticulum (ER) stress response elements, and it has elevated β-catenin and cyclooxygenase-2 (COX-2) levels. Combining FO and Se counteracts the above features of HCC827GR cells, accompanied by the suppression of their raised epithelial-to-mesenchymal transition (EMT) and cancer stem markers, such as vimentin, AXL, N-cadherin, CD133, CD44, and ABCG2. Accordingly, an FO and Se combination augments the gefitinib-mediated growth inhibition and apoptosis of HCC827GR cells, along with the enhanced activation of caspase -3, -9, and ER stress-related caspase-4. Intriguingly, gefitinib further increases the elevated ABCG2 and cancer stem-like side population in HCC827GR cells, which can also be diminished by the FO and Se combination. The results suggest the potential of combining FO and Se in relieving the acquired resistance of NSCLC patients to targeted therapy.
    Type of Medium: Online Resource
    ISSN: 1660-3397
    URL: Article
    DOI: 10.3390/md18080399
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
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  • 8
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    MicroRNA-485-5p targets keratin 17 to regulate oral cancer stemness and chemoresistance via the integrin/FAK/Src/ERK/β-catenin pathway
    Springer Science and Business Media LLC ; 2022
    In:  Journal of Biomedical Science Vol. 29, No. 1 ( 2022-12)
    Details
    In: Journal of Biomedical Science, Springer Science and Business Media LLC, Vol. 29, No. 1 ( 2022-12)
    Abstract: The development of drug resistance in oral squamous cell carcinoma (OSCC) that frequently leads to recurrence and metastasis after initial treatment remains an unresolved challenge. Presence of cancer stem cells (CSCs) has been increasingly reported to be a critical contributing factor in drug resistance, tumor recurrence and metastasis. Thus, unveiling of mechanisms regulating CSCs and potential targets for developing their inhibitors will be instrumental for improving OSCC therapy. Methods siRNA, shRNA and miRNA that specifically target keratin 17 (KRT17) were used for modulation of gene expression and functional analyses. Sphere-formation and invasion/migration assays were utilized to assess cancer cell stemness and epithelial mesenchymal transition (EMT) properties, respectively. Duolink proximity ligation assay (PLA) was used to examine molecular proximity between KRT17 and plectin, which is a large protein that binds cytoskeleton components. Cell proliferation assay was employed to evaluate growth rates and viability of oral cancer cells treated with cisplatin, carboplatin or dasatinib. Xenograft mouse tumor model was used to evaluate the effect of KRT17- knockdown in OSCC cells on tumor growth and drug sensitization. Results Significantly elevated expression of KRT17 in highly invasive OSCC cell lines and advanced tumor specimens were observed and high KRT17 expression was correlated with poor overall survival. KRT17 gene silencing in OSCC cells attenuated their stemness properties including markedly reduced sphere forming ability and expression of stemness and EMT markers. We identified a novel signaling cascade orchestrated by KRT17 where its association with plectin resulted in activation of integrin β4/α6, increased phosphorylation of FAK, Src and ERK, as well as stabilization and nuclear translocation of β-catenin. The activation of this signaling cascade was correlated with enhanced OSCC cancer stemness and elevated expression of CD44 and epidermal growth factor receptor (EGFR). We identified and demonstrated KRT17 to be a direct target of miRNA-485-5p. Ectopic expression of miRNA-485-5p inhibited OSCC sphere formation and caused sensitization of cancer cells towards cisplatin and carboplatin, which could be significantly rescued by KRT17 overexpression. Dasatinib treatment that inhibited KRT17-mediated Src activation also resulted in OSCC drug sensitization. In OSCC xenograft mouse model, KRT17 knockdown significantly inhibited tumor growth, and combinatorial treatment with cisplatin elicited a greater tumor inhibitory effect. Consistently, markedly reduced levels of integrin β4, active β-catenin, CD44 and EGFR were observed in the tumors induced by KRT17 knockdown OSCC cells. Conclusions A novel miRNA-485-5p/KRT17/integrin/FAK/Src/ERK/β-catenin signaling pathway is unveiled to modulate OSCC cancer stemness and drug resistance to the common first-line chemotherapeutics. This provides a potential new therapeutic strategy to inhibit OSCC stem cells and counter chemoresistance.
    Type of Medium: Online Resource
    ISSN: 1423-0127
    URL: Article
    DOI: 10.1186/s12929-022-00824-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
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  • 9
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    Intervention of AXL in EGFR Signaling via Phosphorylation and Stabilization of MIG6 in Non-Small Cell Lung Cancer
    MDPI AG ; 2023
    In:  International Journal of Molecular Sciences Vol. 24, No. 19 ( 2023-10-04), p. 14879-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 24, No. 19 ( 2023-10-04), p. 14879-
    Abstract: About 80% of lung cancer patients are diagnosed with non–small cell lung cancer (NSCLC). EGFR mutation and overexpression are common in NSCLC, thus making EGFR signaling a key target for therapy. While EGFR kinase inhibitors (EGFR–TKIs) are widely used and efficacious in treatment, increases in resistance and tumor recurrence with alternative survival pathway activation, such as that of AXL and MET, occur frequently. AXL is one of the EMT (epithelial–mesenchymal transition) signature genes, and EMT morphological changes are also responsible for EGFR–TKI resistance. MIG6 is a negative regulator of ERBB signaling and has been reported to be positively correlated with EGFR–TKI resistance, and downregulation of MIG6 by miR–200 enhances EMT transition. While MIG6 and AXL are both correlated with EMT and EGFR signaling pathways, how AXL, MIG6 and EGFR interplay in lung cancer remains elusive. Correlations between AXL and MIG6 expression were analyzed using Oncomine or the CCLE. A luciferase reporter assay was used for determining MIG6 promoter activity. Ectopic overexpression, RNA interference, Western blot analysis, qRT–PCR, a proximity ligation assay and a coimmunoprecipitation assay were performed to analyze the effects of certain gene expressions on protein–protein interaction and to explore the underlying mechanisms. An in vitro kinase assay and LC–MS/MS were utilized to determine the phosphorylation sites of AXL. In this study, we demonstrate that MIG6 is a novel substrate of AXL and is stabilized upon phosphorylation at Y310 and Y394/395 by AXL. This study reveals a connection between MIG6 and AXL in lung cancer. AXL phosphorylates and stabilizes MIG6 protein, and in this way EGFR signaling may be modulated. This study may provide new insights into the EGFR regulatory network and may help to advance cancer treatment.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms241914879
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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  • 10
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    Abstract A29: Differential regulation of apoptosis and senescence by the miR-449 family microRNAs and its implications in tumor microenvironments of NSCLC
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 8_Supplement ( 2020-04-15), p. A29-A29
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 8_Supplement ( 2020-04-15), p. A29-A29
    Abstract: MicroRNAs (miRNAs) play important roles in various biologic processes, and aberrant miRNA expression is one of the mechanisms of tumorigenesis. Previous studies indicate that oncogenic HPV infection interrupts the expression of tumor-suppressive miR-34a and contributes to the development of cervical cancer. In addition, the traditional Chinese medicine Gynostemma pentaphyllum (Thunb.) Makino may exert its pharmacologic effects through modifying the gut microbiota by regulating hepatic miR-34a expression. MiR-449 miRs are members of the tumor suppressor miR-34 family and are evolutionarily conserved. In this study, we demonstrated that, in lung cancer cells, ectopic expression of miR-449 family, including miR-449a, miR-449b, and miR-449c, decreased the levels of several G1 phase proteins including cyclin D1, cyclin D3, CDK4, and CDK6 via directly targeting their mRNA’s 3’-UTR. We also observed a differential induction of apoptosis vs. senescence by the miR-449 cluster. While miR-449a and miR-449c induced senescence, miR-449b induced apoptosis and sensitized cancer cells to apoptotic stimuli, such as serum deprivation. Interestingly, among this cluster miRNAs, only miR-449a could induce significant senescence-associated secretory phenotype (SASP), e.g., expression of IL-8, IL-6, IL-1b, and TNF-alpha. Moreover, we also found that miR-449a increased NF-kB phosphorylation at S276, but not phosphorylation site of S536, and promoted the expression of IL-8 mRNA. In this regard, the gut microbiota has been indicated to induce proinflammatory cytokines such as IL-8 to influence the outcomes of cancer patients. In addition to MRX34 (a miR-34a mimic) used in clinical trials, miR-449 family may also potentially become a new therapeutic candidate for NSCLC and other solid tumors’ treatment. Citation Format: Chun-Yu Cho, Shih-Ying Chung, Shuang-En Chuang. Differential regulation of apoptosis and senescence by the miR-449 family microRNAs and its implications in tumor microenvironments of NSCLC [abstract]. In: Proceedings of the AACR Special Conference on the Microbiome, Viruses, and Cancer; 2020 Feb 21-24; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2020;80(8 Suppl):Abstract nr A29.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.MVC2020-A29
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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