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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.1
- 수록면
- 867 - 885 (19page)
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Purpose Caspase recruitment domain containing protein 9 (CARD9) has been demonstrated to be a pro-tumor factor in various cancers. However, our previous study found a significant decrease of CARD9 in malignant pleural effusion compared with benign pleural effusion. So we investigated the role of CARD9 in non-small cell lung cancer (NSCLC) and its working mechanism. Materials and Methods Immunohistochemistry, western blot, and quantitative real-time polymerase chain reaction were used to detect the expression of CARD9 in specimens of NSCLC patients. The Cancer Genome Atlas (TCGA) database was also used to analyze the expression of CARD9 in NSCLC and its predicting value for prognosis. Immunofluorescence was used for CARD9 cellular location. Cell growth assay, clonal formation assay, wound healing assay, matrigel invasion assay, and flow cytometry were used to test cell proliferation, migration, invasion, apoptosis, and cycle progression of NSCLC cells with CARD9 knockdown or CARD9 overexpression. Co-immunoprecipitation was used to identify the interaction between CARD9 and B-cell lymphoma 10 (BCL10). SB203580 was used to inhibit p38 activation. Results CARD9 was decreased in NSCLC tissues compared with normal tissues; low CARD9 expression was associated with poor survival. CARD9 was expressed both in tumor cells and macrophages. Downregulation of CARD9 in NSCLC cells enhanced the abilities of proliferation, invasion, and migration via activated mitogen-activated protein kinases (MAPK)/p38 signaling, while overexpression of CARD9 presented antitumor effects. BCL10 was identified to interact with CARD9. Conclusion We demonstrate that CARD9 is an independent prognostic factor in NSCLC patients and inhibits proliferation, migration, and invasion by suppressing MAPK/p38 pathway in NSCLC cells.
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참고문헌 (27)
참고문헌 신청
Bray F / 2018 / Global cancer statistics 2018 : GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries / CA Cancer J Clin 68:394~424
American Cancer Society / Cancer facts and figures 2019
Hsu YM / 2007 / The adaptor protein CARD9 is required for innate immune responses to intracellular pathogens / Nat Immunol 8:198~205
Yang H / 2007 / pVHL acts as an adaptor to promote the inhibitory phosphorylation of the NF-kappaB agonist Card9 by CK2 / Mol Cell 28:15~27
Cao Z / 2015 / Ubiquitin ligase TRIM62 regulates CARD9-mediated anti-fungal immunity and intestinal inflammation / Immunity 43:715~726
American Cancer Society / Cancer facts and figures 2019
Hsu YM / 2007 / The adaptor protein CARD9 is required for innate immune responses to intracellular pathogens / Nat Immunol 8:198~205
Yang H / 2007 / pVHL acts as an adaptor to promote the inhibitory phosphorylation of the NF-kappaB agonist Card9 by CK2 / Mol Cell 28:15~27
Cao Z / 2015 / Ubiquitin ligase TRIM62 regulates CARD9-mediated anti-fungal immunity and intestinal inflammation / Immunity 43:715~726
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