These results indicate that the cholesterol trafficking defect in NPC disease results in reduced activity of ABCA1, which we suggest is responsible for the low HDL-cholesterol in the majority of NPC subjects and partially responsible for the overaccumulation of cellular lipids in this disorder.
In this study, using MRP overexpressing multidrug resistant nasopharyngeal cancer cells, we examined the expression of apoptosis related genes including p53, p21WAF1, bax and bcl-Xs between drug sensitive KB and its resistant KB/7D cells.
FBW7 increases drug sensitivity to cisplatin in human nasopharyngeal carcinoma by downregulating the expression of multidrug resistance-associated protein.
The expression of c-Myc and ABCG2 was higher in <i>RARS-MAD1L1</i>-positive HNC samples than in negative samples.<b>Conclusions:</b> Our findings indicate that RARS-MAD1L1 might contribute to tumorigenesis, CSC-like properties, and therapeutic resistance, at least in part, through the FUBP1/c-Myc axis, implying that <i>RARS-MAD1L1</i> might serve as an attractive target for therapeutic intervention for NPC.<i></i>.
The prognostic value of ABO blood group may be limited for patients with NPC in the era of IMRT, and no substantial correlation between ABO blood group and plasma EBV DNA was observed.
<b>Objectives</b>: To evaluate the prognostic significance of Adult Comorbidity Evaluation-27 (ACE-27) for elderly patients (age ≥70 years) with locoregionally advanced nasopharyngeal carcinoma (NPC) treated with Intensity-Modulated Radiotherapy (IMRT), with or without chemotherapy.
Compared to NPC patients with low-grade (stage I-II) tumor node metastasis (TNM) and those without lymph node metastasis, the expression of CXCR4, CXCR7, and CXCL12 were significantly higher in NPC patients with high-grade (stage III-IV) TNM and those with lymph node metastasis (P < 0.05).
In conclusion, the loss of ACKR4 promoted CCL21-mediated NPC development; thus, neutralizing CCL21 in NPC with low ACKR4 expression may be a novel treatment strategy.
Using stably transfected MTA1 knockdown or overexpression cells, we discovered the function of MTA1 in actin cytoskeleton reorganization and metastasis processing of NPC in this study.
Using microarray analysis, we also found a reduction in expression of key actin dynamics regulators and several epithelial-to-mesenchymal transition-related genes in G(alpha)(12)-depleted NPC cells.