[High LINC00626 expression promotes esophagogastric junction adenocarcinoma metastasis: the mediating role of the JAK1/STAT3/KHSRP axis].

Q3 Medicine Nan fang yi ke da xue xue bao = Journal of Southern Medical University Pub Date : 2024-03-20 DOI:10.12122/j.issn.1673-4254.2024.03.16

F Zhang, L Fan, X Kang, H Wei, L Li

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Abstract

Objective: To investigate the role of JAK1/STAT3/KHSRP axis in mediating the regulatory effect of LINC00626 on progression of esophagogastric junction adenocarcinoma.

Methods: We collected surgical tumor and adjacent tissue specimens from 64 patients with esophagogastric junction adenocarcinoma and examined the expression levels of LINC00626 and KHSRP. qRT-PCR was used to detect the expressions of LINC00626 and KHSRP in 6 esophageal adenocarcinoma cell lines (OE-19, TE-7, Bic-1, Flo-1, SK-GT-4, and BE-3) and a normal esophageal epithelial cell line (HET-1A). OE-19 and TE-7 cell lines with stable LINC00626 knockdown and FLO-1 and SK-GT-4 cells stably overexpressing LINC00626 were constructed by lentiviral transfection, and the changes in proliferation, migration and invasion of the cells were evaluated using Cell Counting Kit-8 (CCK-8) assay and Transwell migration/invasion assay. The expressions of KHSRP and JAK/STAT pathway proteins in the transfected cells were detected with Western blotting. The effects of LINC006266 knockdown and overexpression on subcutaneous tumor formation and lung metastasis of OE-19 and FLO-1 cell xenografts were tested in nude mice.

Results: The expression levels of LINC00626 and KHSRP were significantly increased in esophagogastric junction adenocarcinoma tissues and in esophageal adenocarcinoma cells. LINC00626 knockdown obviously inhibited the proliferation, migration and invasion of esophageal adenocarcinoma cells in vitro and decreased their tumor formation and lung metastasis abilities in nude mice, while overexpression of LINC00626 produced the opposite effects. In esophageal adenocarcinoma cells, LINC0626 knockdown significantly decreased and LINC00626 overexpression strongly enhanced the phosphorylation of JAK1 and STAT3.

Conclusion: High LINC00626 expression promotes esophageal-gastric junction adenocarcinoma metastasis by activating the JAK1/STAT3/KHSRP signal axis.

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[LINC00626高表达促进食管胃交界处腺癌转移：JAK1/STAT3/KHSRP轴的中介作用】。］

目的研究JAK1/STAT3/KHSRP轴在介导LINC00626对食管胃交界处腺癌进展的调控作用：采用qRT-PCR方法检测LINC00626和KHSRP在6个食管腺癌细胞系（OE-19、TE-7、Bic-1、Flo-1、SK-GT-4和BE-3）和一个正常食管上皮细胞系（HET-1A）中的表达。通过慢病毒转染构建了稳定敲除LINC00626的OE-19和TE-7细胞系以及稳定过表达LINC00626的FLO-1和SK-GT-4细胞系，并使用细胞计数试剂盒-8（CCK-8）检测法和Transwell迁移/侵袭检测法评估了细胞的增殖、迁移和侵袭变化。用 Western 印迹法检测转染细胞中 KHSRP 和 JAK/STAT 通路蛋白的表达。在裸鼠体内检测了 LINC006266 敲除和过表达对 OE-19 和 FLO-1 细胞异种移植的皮下肿瘤形成和肺转移的影响：结果：LINC00626和KHSRP在食管胃交界处腺癌组织和食管腺癌细胞中的表达水平明显升高。敲除 LINC00626 能明显抑制食管腺癌细胞在体外的增殖、迁移和侵袭，降低其在裸鼠体内的肿瘤形成和肺转移能力，而过表达 LINC00626 则产生相反的效果。在食管腺癌细胞中，LINC0626敲除会显著降低JAK1和STAT3的磷酸化，而LINC00626过表达则会强烈增强JAK1和STAT3的磷酸化：结论：LINC00626的高表达通过激活JAK1/STAT3/KHSRP信号轴促进食管胃交界处腺癌的转移。

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