Constructing a Ferroptosis-related Long Non-coding RNA Signature to Predict the Prognostic of Head and Neck Squamous Cell Carcinoma Patients by Bioinformatic Analysis.

Ferroptosis is a novel discovered iron-dependent mode of regulated cell death (RCD) which characterized non-apoptosis. Researches have shown the effect of ferroptosis in the biological activities of tumors. But there is no relevant study showing the relationship between ferroptosis-related genes and head and neck squamous cell carcinoma (HNSCC).

Fibroangiolipoma of palatine tonsil: A case report and literature review.

Lipomas of the palatine tonsil are rare benign neoplasms in clinical practice. We present a case of palatine tonsillar fibroangiolipoma in a 50-year-old Chinese male with a history of multiple lipomas on the back and extremities. It was diagnosed based on histological examination and integrated analysis.

MicroRNA-379-5p/YBX1 Axis Regulates Cellular EMT to Suppress Migration and Invasion of Nasopharyngeal Carcinoma Cells.

Background: Epithelial-mesenchymal transition (EMT) is a major actor modulating the metastasis of nasopharyngeal carcinoma (NPC). Increasing evidence indicates that microRNAs (miRs) are the important regulators of EMT program. However, the potential roles and underlying mechanisms of miR‑379-5p in regulating EMT of NPC cells remain unclear.

Long non-coding RNA 319 facilitates nasopharyngeal carcinoma carcinogenesis through regulation of miR-1207-5p/KLF12 axis.

Long non-coding RNAs (lncRNAs) have been wildly verified to modulate multiple tumorigeneses, especially nasopharyngeal carcinoma (NPC). In present study, we aim to investigate the role of LINC00319 in the NPC carcinogenesis. It was indicated that LINC00319 was markedly increased in NPC tissues and cells in comparison to their corresponding controls.

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p.

Long non-coding RNA (lncRNA) Ewing sarcoma associated transcript 1 (EWSAT1) has been identified as an oncogene, and its dysregulation is closed corrected with tumor progression in Ewing sarcoma. Recently, high-through put analysis reveals that EWSAT1 is also highly expressed in human nasopharyngeal carcinoma (NPC). However, whether the aberrant expression of EWSAT1 in NPC is corrected with malignancy or prognosis has not been expounded.

Effects of TESTIN gene expression on proliferation and migration of the 5-8F nasopharyngeal carcinoma cell line.

Purpose: To investigate effects of the TESTIN (TES) gene on proliferation and migration of highly metastatic nasopharyngeal carcinoma cell line 5-8F and the related mechanisms.

Materials And Methods: The target gene of human nasopharyngeal carcinoma cell line 5-8F was amplified by PCR and cloned into the empty plasmid pEGFP-N1 to construct a eukaryotic expression vector pEGFP-N1-TES. This was then transfected into 5-8F cells.

Picropodophyllin inhibits tumor growth of human nasopharyngeal carcinoma in a mouse model.

Insulin-like growth factor-1 receptor (IGF-1R) is a cell membrane receptor with tyrosine kinase activity and plays important roles in cell transformation, tumor growth, tumor invasion, and metastasis. Picropodophyllin (PPP) is a selective IGF-1R inhibitor and shows promising antitumor effects for several human cancers. However, its antitumor effects in nasopharyngeal carcinoma (NPC) remain unclear.

Targeting the insulin-like growth factor-1 receptor by picropodophyllin as a treatment option for glioblastoma.

Glioblastoma (GB) is the most common malignant brain tumor in adults. It has limited treatment opportunities and is almost exclusively fatal. Owing to the central role the insulin-like growth factor-1 receptor (IGF-1R) plays in malignant cells, it has been suggested as a target for anticancer therapy including GB.

[Expression and clinical significance of insulin like growth factor-1 protein in nasopharyngeal carcinoma].

Objective: To evaluate the expression of IGF-1R protein and its clinical signification in nasopharyngeal carcinoma.

Method: SP immunohistochemical staining was performed to detect the expression of IGF-1R in 63 cases of NPC and 21 inflammatory nasopharyngeal mucosa; and the expression of IGF-1R in three NPC cell lines and chronic nasopharyngitis tissues was examined by western blots.

Result: The positive rates of IGF-1R were 82.

Insulin-like growth factor type-I receptor-dependent phosphorylation of extracellular signal-regulated kinase 1/2 but not Akt (protein kinase B) can be induced by picropodophyllin.

The initial event upon binding of insulin-like growth factor 1 to the insulin-like growth factor type-I receptor (IGF-1R) is auto-phosphorylation of tyrosine residues within the activation loop of the kinase domain followed by phosphorylation of other receptor tyrosine residues and the subsequent activation of the intracellular signaling cascades. We found recently that the cyclolignan picropodophyllin (PPP) inhibits phosphorylation of IGF-1R and phosphatidyl-3 kinase/Akt (protein kinase B) signaling molecules without interfering with the highly homologous insulin receptor. Furthermore, PPP causes regression of tumor grafts and substantially prolongs the survival of animals with systemic tumor disease.

[Expression of BAG-1 and p53 in laryngeal squamous cell carcinoma and their clinical significance].

Objective: To study the expression of BAG-1 and p53 in laryngeal squamous cell carcinoma (LSCC), and the relation between BAG-1 and p53.

Method: BAG-1 and p53 protein were examined by using the method of immunohistochemical SP staining method in 40 cases of LSCC, 27 cases of pap- a-cancerous tissues and 20 cases of polyp specimens from vocal cord tissues.

Result: The positive expression of BAG-1 in.

Expression and growth dependency of the insulin-like growth factor I receptor in craniopharyngioma cells: a novel therapeutic approach.

Craniopharyngioma is a rare benign intracranial epithelial tumor that, however, often recurs and sometimes kills the affected patients, one-third of which are children. In many cases, the patients acquire growth hormone deficiency and postoperatively need substitution. Generally, growth hormone promotes local release of insulin-like growth factor I (IGF-I), which in turn activates the IGF-I receptor (IGF-IR) if present.