Our study confirmed STIL as a key regulator that promotes the proliferation of NPC, providing insight into the molecular mechanisms of nasopharyngeal carcinoma and suggesting a novel therapeutic strategy.
Importantly, high ICOS expression is significantly correlated with overall survival (OS) of NPC patients (N = 185, p < 0.001), and ICOS expression is also proved to be an independent prognostic factor by multivariate analysis.
We found that DLX6-AS1 was a cancer-promoting lncRNA to facilitate the progression of NPC, and its underlying mechanism was suppressing miR-199a-5p expression.
We further found that PVT1 serves as a scaffold for the chromatin modification factor KAT2A, which mediates histone 3 lysine 9 acetylation (H3K9), recruiting the nuclear receptor binding protein TIF1β to activate NF90 transcription, thereby increasing HIF-1α stability and promoting a malignant phenotype in NPC cells.
Vascular endothelial growth factor C (VEGF-C) has been reported to be responsible for the lymphatic vessel density, tumor staging and lymph node metastasis, resulting in the failure of nasopharyngeal carcinoma (NPC) after radiotherapy.
Our result indicated that a panel including five serum protein (SPARC SERPIND1 C4B PPIB FAM173A) based on serum proteomics provided a high discrimination ability for radiotherapy effects in NPC patients.
This is a retrospective uncontrolled case series review of patients who were investigated for suspected nasopharyngeal carcinoma between 2009 and 2017 at York Teaching Hospital NHS Foundation Trust.
In summary, our works suggested that these novel 4-aniline-thieno[2,3-d]pyrimidine based MNK1 inhibitors might be attractive lead compounds for targeted therapy of renal cell carcinoma and nasopharyngeal carcinoma.
In the present study, biopsies from untreated NPC were obtained and subjected to multicolor flow-cytometry focusing on DC subtype markers: CD123 for plasmacytoid DCs (pDCs); and CD1c and CD141 for myeloid DCs (mDCs).