Year-end Sale % OFF 
Abstract
Metastasis is the major cause of treatment failure in patients with nasopharyngeal carcinoma (NPC). However, the molecular mechanisms of NPC metastasis are poorly understood. Here, using our customized gene microarray containing all of the known human transcription factors and the current markers for epithelial-mesenchymal transition, we report that TEL2 was down-regulated in highly metastatic NPC cells and the metastatic tissues in lymph node. Mechanistically, TEL2 inhibits the cell migration and invasion in vitro and metastasis in vivo by directly suppressing the SERPINE1 promoter in NPC. Consistently, an inverse correlation was observed between the protein levels of TEL2 and SERPINE1 using clinical NPC samples. Collectively, we have provided the first evidence that TEL2 plays a key role in NPC metastasis by directly down-regulating SERPINE1, and that this novel axis of TEL2 / SERPINE1 may be valuable to develop new strategies for treating NPC patients with metastasis.
Highlights
Nasopharyngeal carcinoma (NPC), originating from the nasopharynx, is highly prevalent in Southern China and Southeast Asia with an incidence rate of 15–50/100,000 [1,2,3,4]
We demonstrate that TEL2 plays a key role in NPC metastasis by directly down-regulating SERPINE1, and that this novel axis of TEL2 / SERPINE1 may be valuable to develop new strategies for treating NPC patients with metastasis
Many of these gene expressions were different between the primary tumor and the lymph node (LN) and/or those of S26 and S18, as shown in Supplemental Table 1, there were only small percentages of genes simultaneously altered in both sets of screens, including the well-known markers for epithelial-mesenchymal transition (EMT) and/ or metastasis, such as Snail, Twist and Zeb1, indicating that this strategy was suitable to look for new regulators for NPC metastasis
Summary
Nasopharyngeal carcinoma (NPC), originating from the nasopharynx, is highly prevalent in Southern China and Southeast Asia with an incidence rate of 15–50/100,000 [1,2,3,4]. Distant metastasis is the major cause of treatment failure for NPC patients [1, 3, 5, 6]. To determine the roles of these factors in NPC metastasis, we have generated the customized gene microarray containing all of the known human transcription factors and the current markers for epithelial-mesenchymal transition (EMT). Using this special microarray, TEL2, an ETS family whose members have key roles in cancer metastasis [12,13,14,15], was identified as an important regulator of NPC metastasis
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
