Chen Qian, He Xiao, Li Bin, Chen Jingjing, Tang Xuxia
Department of Otolaryngology, The First Affiliated Hospital of Zhejiang Traditional Chinese Medical University, Hangzhou 310006, China.
Evid Based Complement Alternat Med. 2022 Jul 5;2022:1562219. doi: 10.1155/2022/1562219. eCollection 2022.
This study aimed to explore the function and molecular mechanism of long noncoding RNA Small Nucleolar RNA Host Gene 1 (SNHG1) in the development of hypopharyngeal squamous cell carcinoma (HSCC).
Human HSCC cell line FaDu was used in this study. Cell viability and apoptosis were detected using CCK-8 assay and flow cytometry, respectively. Cell migration and invasion were measured by Transwell assay. The expression of PARP6, XRCC6, -catenin, and EMT-related proteins (E-cadherin and N-cadherin) were determined using western blotting. Moreover, the regulatory relationship between SNHG1 and PARP6 was investigated. Furthermore, the effects of the SNHG1/PARP6 axis on tumorigenicity were explored .
Suppression of SNHG1 suppressed the viability, migration, and invasion but promoted apoptosis of FaDu cells ( < 0.01). PARP6 is a target of SNHG1, which was upregulated by SNHG1 knockdown in FaDu cells ( < 0.01). SNHG1 suppression and RARP6 overexpression inhibited FaDu cell proliferation, migration, and invasion ( < 0.05). SNHG1 suppression and RARP6 overexpression also inhibited tumorigenicity of HSCC . Furthermore, the protein expression of E-cadherin was significantly increased and that of N-cadherin, -catenin, and XRCC6 was dramatically decreased in HSCC after SNHG1 suppression or/and RARP6 overexpression both and ( < 0.01).
SNHG1 silencing inhibits HSCC malignant progression via upregulating PARP6. XRCC6/-catenin/EMT axis may be a possible downstream mechanism of the SNHG1/PARP6 axis in HSCC. SNHG1/PARP6 can be used as a promising target for the treatment of HSCC.
本研究旨在探讨长链非编码RNA小核仁RNA宿主基因1（SNHG1）在下咽鳞状细胞癌（HSCC）发生发展中的作用及分子机制。
本研究采用人HSCC细胞系FaDu。分别使用CCK-8法和流式细胞术检测细胞活力和凋亡情况。采用Transwell法检测细胞迁移和侵袭能力。通过蛋白质印迹法检测PARP6、XRCC6、β-连环蛋白和上皮-间质转化（EMT）相关蛋白（E-钙黏蛋白和N-钙黏蛋白）的表达。此外，研究了SNHG1与PARP6之间的调控关系。进一步探讨了SNHG1/PARP6轴对肿瘤发生的影响。
抑制SNHG1可抑制FaDu细胞的活力、迁移和侵袭，但促进其凋亡（P<0.01）。PARP6是SNHG1的靶标，在FaDu细胞中敲低SNHG1可使其上调（P<0.01）。抑制SNHG1和过表达RARP6可抑制FaDu细胞的增殖、迁移和侵袭（P<0.05）。抑制SNHG1和过表达RARP6也可抑制HSCC的肿瘤发生。此外，在体内和体外抑制SNHG1或/和过表达RARP6后，HSCC中E-钙黏蛋白的蛋白表达显著增加，而N-钙黏蛋白、β-连环蛋白和XRCC6的蛋白表达显著降低（P<0.01）。
SNHG1沉默通过上调PARP6抑制HSCC的恶性进展。XRCC6/β-连环蛋白/EMT轴可能是HSCC中SNHG1/PARP6轴的潜在下游机制。SNHG1/PARP6可作为HSCC治疗的一个有前景的靶点。
