Trim44 facilitates the migration and invasion of human lung cancer cells via the NF-κB signaling pathway

Verfasser / Beitragende:
[Qingquan Luo, Hao Lin, Xiangyun Ye, Jia Huang, Shun Lu, Lin Xu]
Ort, Verlag, Jahr:
2015
Enthalten in:
International Journal of Clinical Oncology, 20/3(2015-06-01), 508-517
Format:
Artikel (online)
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024 7 0 |a 10.1007/s10147-014-0752-9  |2 doi 
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245 0 0 |a Trim44 facilitates the migration and invasion of human lung cancer cells via the NF-κB signaling pathway  |h [Elektronische Daten]  |c [Qingquan Luo, Hao Lin, Xiangyun Ye, Jia Huang, Shun Lu, Lin Xu] 
520 3 |a Background: Trim44 is an important member of the tripartite motif-containing protein (TRIM) family. Recent research reported that Trim44 might play an important role in tumorigenesis, although its role in non-small cell lung cancer (NSCLC) and the related mechanisms is not yet known. Methods: In this study we analyzed 30 pairs of NSCLC tumors and the matched adjacent normal tissue to define the relationship between Trim44 and NSCLC tumors. The function of Trim44 in cell migration and invasion was determined by overexpression of Trim44 in normal bronchial epithelial cell line 16HE or knockdown of Trim44 in A549 cells, respectively. Whether Trim44-mediated NF-κB signaling activation was involved in Trim44-mediated promotion of lung cancer was tested by q-PCR analysis and cell migration and invasion assay using PDTC, an inhibitor of NF-κB. Results: We found that Trim44 was upregulated in NSCLC tumors (14/30 cases; 46.7%). Furthermore, Trim44 was upregulated in many NSCLC cell lines, especially in A549 and H441. Moreover, Trim44 significantly enhanced cell migration and invasion ability, which was related to increased CXCR6 and matrix metalloproteinase 9 (MMP9). Knockdown of Trim44 in A549 cells by siRNA showed a diminished effect in cell migration and invasion. Further investigation revealed that blocking the NF-κB signaling pathway using PDTC, an inhibitor of NF-κB, reversed the expression of CXCR6 and MMP9, and alleviated the promotion of migration and invasion mediated by Trim44. Conclusions: Our data suggest that Trim44 promotes NSCLC development through activation of NF-κB signaling via upregulating CXCL16 and MMP9 expression. 
540 |a Japan Society of Clinical Oncology, 2014 
690 7 |a Trim44  |2 nationallicence 
690 7 |a NSCLC  |2 nationallicence 
690 7 |a Migration  |2 nationallicence 
690 7 |a Invasion  |2 nationallicence 
690 7 |a NF-κB  |2 nationallicence 
700 1 |a Luo  |D Qingquan  |u Nanjing Medical University, 210029, Nanjing, China  |4 aut 
700 1 |a Lin  |D Hao  |u Shanghai Lung Tumor Clinical Medical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, 200030, Shanghai, China  |4 aut 
700 1 |a Ye  |D Xiangyun  |u Shanghai Lung Tumor Clinical Medical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, 200030, Shanghai, China  |4 aut 
700 1 |a Huang  |D Jia  |u Shanghai Lung Tumor Clinical Medical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, 200030, Shanghai, China  |4 aut 
700 1 |a Lu  |D Shun  |u Shanghai Lung Tumor Clinical Medical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, 200030, Shanghai, China  |4 aut 
700 1 |a Xu  |D Lin  |u Department of Thoracic Surgery, Nanjing Medical University Affiliated Cancer Hospital, 210009, Nanjing, Jiangsu, China  |4 aut 
773 0 |t International Journal of Clinical Oncology  |d Springer Japan  |g 20/3(2015-06-01), 508-517  |x 1341-9625  |q 20:3<508  |1 2015  |2 20  |o 10147 
856 4 0 |u https://doi.org/10.1007/s10147-014-0752-9  |q text/html  |z Onlinezugriff via DOI 
898 |a BK010053  |b XK010053  |c XK010000 
900 7 |a Metadata rights reserved  |b Springer special CC-BY-NC licence  |2 nationallicence 
908 |D 1  |a research-article  |2 jats 
949 |B NATIONALLICENCE  |F NATIONALLICENCE  |b NL-springer 
950 |B NATIONALLICENCE  |P 856  |E 40  |u https://doi.org/10.1007/s10147-014-0752-9  |q text/html  |z Onlinezugriff via DOI 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Luo  |D Qingquan  |u Nanjing Medical University, 210029, Nanjing, China  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Lin  |D Hao  |u Shanghai Lung Tumor Clinical Medical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, 200030, Shanghai, China  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Ye  |D Xiangyun  |u Shanghai Lung Tumor Clinical Medical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, 200030, Shanghai, China  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Huang  |D Jia  |u Shanghai Lung Tumor Clinical Medical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, 200030, Shanghai, China  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Lu  |D Shun  |u Shanghai Lung Tumor Clinical Medical Center, Shanghai Chest Hospital, Shanghai Jiaotong University, 200030, Shanghai, China  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Xu  |D Lin  |u Department of Thoracic Surgery, Nanjing Medical University Affiliated Cancer Hospital, 210009, Nanjing, Jiangsu, China  |4 aut 
950 |B NATIONALLICENCE  |P 773  |E 0-  |t International Journal of Clinical Oncology  |d Springer Japan  |g 20/3(2015-06-01), 508-517  |x 1341-9625  |q 20:3<508  |1 2015  |2 20  |o 10147