LncRNA TP73-AS1 promotes nasopharyngeal carcinoma progression through targeting miR-342-3p and M2 polarization via exosomes

• Published in: Cancer cell international Vol. 22; no. 1; p. 16
• Main Authors: Yao, Hongchao, Tian, Linli, Yan, Bingrui, Yang, Like, Li, Yushan
• Format: Journal Article
• Language: English
• Published: England BioMed Central 10.01.2022; BMC
• Subjects: Cancer; Cell growth; Cell proliferation; Cloning; DNA biosynthesis; Exosome; Exosomes; Gene expression; Genomes; Laboratory animals; Macrophages; Medical research; miR-342-3p; Molecular modelling; Morphology; Nasopharyngeal carcinoma; Non-coding RNA; Polarization; Primary Research; Progression; Software; Throat cancer; TP73-AS1; Tumorigenesis; Tumors; United States > US; China; Japan; Nasopharyngeal carcinoma; Progression; TP73-AS1; miR-342-3p; Exosome
• ISSN: 1475-2867; 1475-2867
• DOI: 10.1186/s12935-021-02418-5

Nasopharyngeal carcinoma (NPC) is a deadly cancer, mainly presenting in southeast and east Asia. Long noncoding RNAs (lncRNAs) play essential roles in cancer progression. Exosomes are critical for intercellular communication. Thus, the aim of this study was to identify the functional lncRNAs in NPC and its relevant mechanisms. Data from public databases were utilized to screen for functional lncRNAs in NPC. Functional and mechanical experiments were performed to determine the role of lncRNAs in NPC and its relative molecular mechanisms. Exosomes derived from NPC cells were isolated to determine their function in tumor-associated macrophages. LncRNA TP73-AS1 was increased in NPC cells and tissues and was associated with a poor prognosis. TP73-AS1 overexpression promoted proliferation, colony formation, and DNA synthesis of NPC cells while TP73-AS1 knockdown showed opposite roles. TP73-AS1 could directly bind with miR-342-3p. MiR-342-3p overexpression attenuated the effect of TP73-AS1 in NPC cells. Furthermore, TP73-AS1 was transferred by exosomes to promote M2 polarization of macrophages. Lastly, exosomal TP73-AS1 enhanced the motility and tube formation of macrophages. Together, this study suggests that TP73-AS1 promotes NPC progression through targeting miR-342-3p and exosome-based communication with macrophages and that TP73-AS1 might be an emerging biomarker for NPC.