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Background: Long non-coding RNA (lncRNA) LINC01569 plays an important role in regulating the tumor microenvironment (TME) and macrophage polarization. However, whether it participates in the progression of hypopharyngeal carcinoma by regulating the TME remains unclear. Methods: An online database was used to analyze clinical data. Macrophage polarization was detected using qRT-PCR and flow cytometry. In vivo experiments were performed using tumor-bearing nude mice. A co-culture system of hypopharyngeal carcinoma cells and macrophages was used to explore the interactions between the two cell types. Results: LINC01569 enhancement was observed in hypopharyngeal carcinoma tumor-associated macrophages (TAMs). In IL4-induced M2 macrophages, the expression of LINC01569 increased, while LINC01569 expression declined significantly in LPS-induced M1 macrophages. SiRNA-mediated downregulation of LINC01569 inhibits IL4-induced M2 macrophage polarization. Using online databases and a dual-luciferase reporter, miR-193a-5p was confirmed as a potential downstream sponge of LINC01569. MiR-193a-5p expression decreased in IL4-mediated M2 macrophages, which was restored by LINC01569 downregulation. Additionally, LINC01569 inhibition-mediated blocking of M2 macrophage polarization was moderately abolished by transfection with the miR-193a-5p inhibitor. Fatty acid desaturase 1 (FADS1) was verified as a downstream target of miR-193a-5p, and LINC01569 downregulation-mediated inhibition of FADS1 was blocked by miR-193a-5p mimics. Importantly, LINC01569 downregulation-mediated decline in M2 macrophage polarization was abolished by miR-193a-5p mimics, which was further reversed by FADS1 knockdown. Implantation of a mixture of FaDu cells and IL4-induced macrophages promoted tumor growth and proliferation, which were abrogated by the knockdown of LINC01569 in macrophages. Using an in co-culture system of FaDu cells and macrophages in vitro , M2 macrophage-regulated cell growth and apoptosis of FaDu cells were found to be mediated by the LINC01569/miR-193a-5p signaling axis. Conclusion: LINC01569 is highly expressed in the TAMs of hypopharyngeal carcinoma. LINC01569 downregulation restrains macrophages from polarizing toward M2 through the miR-193a-5p/FADS1 signaling axis, thereby helping tumor cells escape inherent immune surveillance and promoting the occurrence and development of hypopharyngeal carcinoma., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Thyroid cancer (THCA) is a common malignancy of the endocrine system which threatens people's health and life quality. It is urgent to find the marker gene of THCA. BHLHE40 is a key gene involved in tumor malignant progression. However, the role of BHLHE40 in THCA remains unclear. In this study, 346 upregulated and 302 downregulated genes were found by analyzing the Gene Expression Omnibus database. BHLHE40 was upregulated in THCA. BHLHE40 and its related differentially expressed genes were involved in cell adhesion and differentiation in THCA. Moreover, BHLHE40 was also highly expressed in THCA cells and tissues. Downregulation of BHLHE40 inhibited cell growth and metastasis. Knockdown of BHLHE40 conditioned media retarded cell migration in M2 macrophages. In addition, knockdown of BHLHE40 inhibited CD206 and CD163 expression and decreased the secretion of interleukin-10 in M2 macrophage. Therefore, BHLHE40 has the potential to be used as a biomarker of immune infiltration and tumorigenesis in THCA., Competing Interests: None