Advances in tumor immune microenvironment of head and neck squamous cell carcinoma: A review of literature.

Squamous cell carcinoma is seen as principal malignancy of head and neck. Tumor immune microenvironment plays a vital role in the occurrence, development and treatment of head and neck squamous cell carcinoma (HNSCC). The effect of immunotherapy, in particular, is closely related to tumor immune microenvironment. This review searched for high-quality literature included within PubMed, Web of Science, and Scopus using the keywords "head and neck cancers," "tumor microenvironment" and "immunotherapy," with the view to summarizing the characteristics of HNSCC immune microenvironment and how various subsets of immune cells promote tumorigenesis. At the same time, based on the favorable prospects of immunotherapy having been shown currently, the study is committed to pinpointing the latest progress of HNSCC immunotherapy, which is of great significance in not only further guiding the diagnosis and treatment of HNSCC, but also conducting its prognostic judgement.

miR-150-5p inhibits nasopharyngeal cancer genesis by suppressing PYCR1.

BACKGROUND: Nasopharyngeal cancer (NPC) is a rare cancer type with a low five-year survival rate. Dysregulation of PYCR1 and miR-150-5p has been involved in the development of various cancers. However, the molecular mechanism of the miR-150-5p-PYCR1 axis in NPC remains unclear. METHODS: The expressions of miR-150-5p and PYCR1 in NPC tissues and cells were measured by RT-qPCR. The luciferase assay and RNA pull-down assay were used to confirm the interaction between miR-150-5p and PYCR1. The function of overexpression of miR-150-5p and PYCR1 were detected by cell viability, proliferation, migration and invasion in NPC C666-1 and SUNE-1 cells. RESULTS: The miR-150-5p expression was reduced in NPC tissues and cells and negatively correlated with PYCR1 level. Upregulation of miR-150-5p conspicuously repressed cell growth. However, upregulation of PYCR1 significantly facilitated the development of NPC, which further suppressed NPC tumorigenesis by abolishing the effect of miR-150-5p. CONCLUSIONS: We clarified that miR-150-5p attenuated NPC tumorigenesis through reducing PYCR1 expression. This provides a new perspective of NPC involving both miR-150-5p and PYCR1 for the treatment of NPC.

MicroRNA hsa-miR-150-5p inhibits nasopharyngeal carcinogenesis by suppressing PYCR1 (pyrroline-5-carboxylate reductase 1).

Nasopharyngeal cancer is a rare cancer type, but with a low five-year survival rate. Dysregulation of pyrroline-5-carboxylate reductase 1 (PYCR1) and microRNA hsa-miR-150-5p is involved in the development of various cancers. However, the molecular mechanism of the hsa-miR-150-5p-PYCR1 axis in nasopharyngeal cancer remains unclear. To identify the mechanism of the hsa-miR-150-5p-PYCR1 axis, the expression of hsa-miR-150-5p and PYCR1 in nasopharyngeal cancer tissues and cells was first measured by reverse transcription quantitative polymerase chain reaction. The luciferase and RNA pull-down assays were used to confirm the interaction between hsa-miR-150-5p and PYCR1. The overexpression of hsa-miR-150-5p and PYCR1 was detected by cell viability, proliferation, western blotting, migration, and invasion in nasopharyngeal cancer cells. The expression levels of hsa-miR-150-5p was reduced in the nasopharyngeal cancer tissues and cells and were negatively correlated with the PYCR1 levels. The upregulation of hsa-miR-150-5p significantly repressed cell growth and promoted apoptosis. However, the upregulation of PYCR1 expression significantly promoted nasopharyngeal carcinogenesis, which could abolish the inhibitory effect of hsa-miR-150-5p. In conclusion, we clarified that hsa-miR-150-5p attenuated nasopharyngeal carcinogenesis by reducing the PYCR1 expression levels. This provides a new perspective of nasopharyngeal cancer involving both hsa-miR-150-5p and PYCR1 for the treatment of nasopharyngeal cancer.

Upregulation of long non coding RNA PCAT-1 contributes to cell proliferation, migration and apoptosis in hepatocellular carcinoma.

Long non-coding RNAs (lncRNAs) exert regulatory functions on various biological processes in cancer cells, including proliferation, apoptosis and mobility. Prostate cancer-associated transcript 1 (PCAT-1) is a novel lncRNA that promotes cell proliferation in prostate cancer, however, the effect of PCAT­1 in hepatocellular carcinoma (HCC) remains to be elucidated. The present study hypothesized that PCAT­1 also exerts an important effect in HCC. The current study investigated PCAT-1 expression levels in HCC tissue samples and HepG2 and Bel­7402 cell lines using the reverse transcription-quantitative polymerase chain reaction. The results demonstrated that PCAT-1 was upregulated in HCC tissue samples and cell lines compared with adjacent non­cancerous tissues and the L02 normal liver epithelial cell line. PCAT­1 suppression using PCAT­1 small hairpin RNA in HepG2 and Bel­7402 cells inhibited cell proliferation and migration, and induced apoptosis. Overexpression of PCAT­1 induced synthetic plasmid vectors was demonstrated to increase cell proliferation and migration, and inhibit apoptosis. Results from the present study suggest that PCAT­1 exerts an oncogenic effect in HCC and silencing PCAT-1 may be a potential novel therapeutic strategy for HCC.