RESUMEN
Fibrinogen-like protein 1 (FGL1) is a proliferation- and metabolism-related factor secreted by the liver that is aberrantly expressed and functionally abnormal in human malignancies. However, the role of FGL1 in head and neck squamous cell carcinoma (HNSCC) remains unknown. We analysed FGL1 expression in HNSCC and its impact on patient survival using the TCGA database. The role of FGL1 in HNSCC cells was investigated by Cell Counting Kit-8, colony formation, and Transwell assays. In addition, we conducted in vivo experiments to assess the effect of FGL1 knockdown on tumour growth. We found that FGL1 was highly expressed in HNSCC and correlated with a poor prognosis. Downregulation of FGL1 expression inhibited the proliferation and invasion of HNSCC cells. Furthermore, mechanistic analysis revealed that FGL1 induced an epithelial-mesenchymal transition (EMT) phenotype and, thus, the malignant progression of HNSCC cells. Finally, xenograft models showed that FGL1 knockdown significantly inhibited EMT in HNSCC in vivo. Our study revealed that FGL1, an oncogene, promotes the malignant progression of HNSCC, providing new perspective on and potential therapeutic target for the treatment of HNSCC.
RESUMEN
Basal cell adenocarcinoma of the submandibular gland is an extremely rare carcinoma of the salivary gland that originates from the basal cells of the submandibular gland. Due to its rarity, there are relatively few case reports and literature on this cancer. After comprehensive clinical, imaging, and pathologic analyses, we confirmed the patient's diagnosis and documented the consultation in detail. The purpose of this article is to report the case of a patient with basal cell adenocarcinoma of the submandibular gland and to perform a review of the relevant literature to improve the understanding of this rare disease.
RESUMEN
PURPOSE: Laryngeal cancer (LC) is one of the most ordinary head and neck cancers worldwide. In this study, the role of long non-coding RNA (lncRNA) PCAT1 in LC was explored. METHODS: PCAT1 expression in 50 paired tissue samples from LC patients was monitored by real-time quantitative polymerase chain reaction (RT-qPCR). Afterwards, function assays were conducted to explore how PCAT1 participated in metastasis of LC in vitro and in vivo. Then, bio-information software and luciferase assay were utilized to predict the possible target microRNA (miR) of PCAT1 in LC. RESULTS: PCAT1 was obviously upregulated in LC tissues compared with adjacent tissues. Knockdown of PCAT1 inhibited the ability of cell migration and invasion in LC. Moreover, knockdown of PCAT1 inhibited tumor formation in vivo. Furthermore, miR-210-3p was sponged by PCAT1 in LC cells. CONCLUSION: PCAT1 was first identified as a novel oncogene in LC and could promote LC cell migration and invasion by sponging miR-210-3p.