Galectin 2 regulates JAK/STAT3 signaling activity to modulate oral squamous cell carcinoma proliferation and migration <i>in vitro</i>

IF 1.8 4区 生物学 Q4 BIOLOGY
XINRU FENG, Luyi Xiao
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引用次数: 11

Abstract

Background: Galectin 2 (LGALS2) is a protein previously reported to serve as a mediator of disease progression in a range of cancers. The function of LGALS2 in oral squamous cell carcinoma (OSCC), however, has yet to be explored, prompting the present study to address this literature gap. Methods: Overall, 144 paired malignant tumor tissues and paracancerous OSCC patient samples were harvested and the LGALS2 expression levels were examined through qPCR and western immunoblotting. The LGALS2 coding sequence was introduced into the pcDNA3.0 vector, to enable the overexpression of this gene, while an LGALS2-specific shRNA and corresponding controls were also obtained. The functionality of LGALS2 as a regulator of the ability of OSCC cells to grow and undergo apoptotic death in vitro was assessed through EdU uptake and CCK-8 assays, and flow cytometer, whereas a Transwell system was used to assess migratory activity and invasivity. An agonist of the Janus Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) pathway was also used to assess the role of this pathway in the context of LGALS2 signaling. Results: Here, we found that lower LGALS2 protein and mRNA expression were evident in OSCC tumor tissue samples, and these expression levels were associated with clinicopathological characteristics and patient survival outcomes. Silencing LGALS2 enhanced proliferation in OSCC cells while rendering these cells better able to resist apoptosis. The opposite was instead observed after LGALS2 was overexpressed. Mechanistically, the ability of LGALS2 to suppress the progression of OSCC was related to its ability to activate the JAK/STAT3 signaling axis. Conclusion: Those results suggest a role for LGALS2 as a suppressor of OSCC progression through its ability to modulate JAK/ STAT3 signaling, supporting the potential utility of LGALS2 as a target for efforts aimed at treating OSCC patients.
半乳糖凝集素2调节JAK/STAT3信号活性,调控口腔鳞状细胞癌体外增殖和迁移
背景:凝集素2 (LGALS2)是一种先前报道的蛋白,可作为一系列癌症疾病进展的介质。然而,LGALS2在口腔鳞状细胞癌(OSCC)中的功能尚未被探索,因此本研究旨在弥补这一文献空白。方法:共收集144例配对的恶性肿瘤组织和癌旁OSCC患者标本,通过qPCR和western免疫印迹法检测LGALS2的表达水平。将LGALS2编码序列导入pcDNA3.0载体中,使该基因过表达,同时获得LGALS2特异性shRNA和相应对照。通过EdU摄取和CCK-8测定以及流式细胞仪评估LGALS2作为体外OSCC细胞生长和凋亡性死亡能力调节剂的功能,而Transwell系统用于评估迁移活性和侵袭性。我们还使用JAK2 / STAT3通路的激动剂来评估该通路在LGALS2信号传导中的作用。结果:我们发现,在OSCC肿瘤组织样本中,LGALS2蛋白和mRNA的表达明显降低,并且这些表达水平与临床病理特征和患者生存结果相关。沉默LGALS2增强了OSCC细胞的增殖,同时使这些细胞能够更好地抵抗凋亡。LGALS2过表达后则相反。从机制上讲,LGALS2抑制OSCC进展的能力与其激活JAK/STAT3信号轴的能力有关。结论:这些结果表明LGALS2通过其调节JAK/ STAT3信号传导的能力,作为OSCC进展的抑制因子,支持LGALS2作为治疗OSCC患者的靶点的潜在用途。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biocell
Biocell 生物-生物学
CiteScore
1.50
自引率
16.70%
发文量
259
审稿时长
>12 weeks
期刊介绍: BIOCELL welcomes Research articles and Review papers on structure, function and macromolecular organization of cells and cell components, focusing on cellular dynamics, motility and differentiation, particularly if related to cellular biochemistry, molecular biology, immunology, neurobiology, and on the suborganismal and organismal aspects of Vertebrate Reproduction and Development, Invertebrate Biology and Plant Biology.
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