Galectin‑3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma.
Galectin‑3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma.
复制标题
DOI：
10.3892/mmr.2021.12009
复制
发表时间：
2021-05
影响因子：
3.4
通讯作者：
Tang CE
中科院分区：
文献类型：
--
作者：
Li M;Chen YB;Liu F;Qu JQ;Ren LC;Chai J;Tang CE
鼻咽癌（Nasopharyngeal carcinoma，NPC）是一种起源于鼻咽粘膜组织的上皮性癌，在东南亚非常流行。半乳糖凝集素-3（gal-3）在许多癌症中起关键作用，但其在NPC中的作用仍有待阐明。本研究旨在探讨gal-3在鼻咽癌中的作用。采用免疫组化和ELISA法检测鼻咽癌和慢性鼻炎（CR）患者组织中gal-3的表达水平。建立了Gal-3短发夹RNA（sh RNA），在5- 8 F和6- 10 B细胞中敲低gal-3，以评估gal-3在NPC细胞系增殖、迁移和凋亡中的作用。采用免疫组化法检测肿瘤组织中IL-6、IL-8的表达情况，并分析其与gal-3表达的相关性。结果表明，与CR患者相比，NPC患者中gal-3表达上调。gal-3的敲低抑制了5- 8 F和6- 10 B细胞的增殖和迁移，并促进了这些细胞的凋亡。5- 8 F和6- 10 B细胞转染gal-3 shRNA后MMP-9和IL-8的表达水平也明显降低。gal-3的表达水平与鼻咽癌的炎症状态呈正相关。在5- 8 F和6- 10 B细胞中，gal-3基因敲低后ERK 1/2和Akt的磷酸化水平下调。结论：gal-3在鼻咽癌组织中表达上调，且与鼻咽癌的炎症状态呈正相关。结果表明，gal-3能促进5- 8 F和6- 10 B细胞的增殖和迁移，并抑制其凋亡。Gal-3对鼻咽癌细胞的作用机制可能与ERK 1/2和Akt的激活有关。
Nasopharyngeal carcinoma (NPC) is an epithelial carcinoma originating from the nasopharyngeal mucosal tissue and is highly prevalent in southeast Asia. Galectin-3 (gal-3) serves crucial roles in many cancers but its role in NPC remains to be elucidated. The aim of the present study was to investigate the role of gal-3 in NPC. Immunohistochemistry and ELISA were used to determine the expression level of gal-3 in patients with NPC or chronic rhinitis (CR). Gal-3 short hairpin (sh)RNA was established to knockdown gal-3 in 5–8F and 6–10B cells, allowing for the evaluation of the roles of gal-3 in proliferation, migration and apoptosis in NPC cell lines. Immunohistochemistry staining of IL-6 and IL-8 was applied to access the inflammatory state of tumor tissues, and the correlation between the inflammatory state and gal-3 was analyzed. The results demonstrated that gal-3 was upregulated in patients with NPC compared with patients with CR. Knockdown of gal-3 inhibited proliferation and migration in 5-8F and 6-10B cells, as well as promoted apoptosis in these cells. The expression levels of MMP-9 and IL-8 were also decreased in 5-8F and 6-10B cells after transfection with gal-3 shRNA. A positive correlation was identified between the expression level of gal-3 and the inflammatory state of NPC. The phosphorylation levels of ERK1/2 and Akt were downregulated after knockdown of gal-3 in 5-8F and 6-10B cells. In conclusion, the expression level of gal-3 was upregulated in patients with NPC and was positively correlated with the inflammatory state of NPC. The results suggested that gal-3 promoted the proliferation and migration of 5-8F and 6-10B cells, while inhibiting the apoptosis of these cells. Moreover, activation of ERK1/2 and Akt may be the underlying mechanism of the effects of gal-3 on NPC.