KLF5 通过转录激活 FGFBP1 促进食管鳞癌。
KLF5 promotes esophageal squamous cell cancer through the transcriptional activation of FGFBP1.
机构信息
Department of Oncology, First Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science & Technology, Baotou, Inner Mongolia, China.
Imaging Department, Third Affiliated Hospital of Baotou Medical College, Baotou, Inner Mongolia, China.
出版信息
Med Oncol. 2023 Dec 12;41(1):17. doi: 10.1007/s12032-023-02244-x.
Krüpple-like factor 5 (KLF5) is a zinc-finger-containing transcription factor implicated in several human malignancies, but its potential regulatory mechanisms implicated in esophageal squamous cell carcinoma (ESCC) remain elusive. Here, we show that KLF5 is upregulated in ESCC, where its level was significantly associated with tumor differentiation and lymph node metastasis status. Upregulated KLF5 expression promoted the proliferation, migration, and invasion of ESCC cells. Reduced KLF5 showed the opposite effects. Mechanistically, KLF5 exerts its tumor promotion effect by up-regulating fibroblast growth factor binding protein 1 (FGF-BP1) and snail family transcriptional repressor 2 (SNAIL2). KLF5 binds to the promoter regions of FGF-BP1 and transcriptionally activates its expression. Our study indicated that KLF5 could promote esophageal squamous cell cancer proliferation, migration, and invasion by upregulating FGF-BP1/SNAIL2 signaling. Our work suggests that KLF5 might be a proto-oncogene in ESCC and implicated in ESCC metastasis.
锌指转录因子 5（Krüpple-like factor 5，KLF5）在多种人类恶性肿瘤中被认为是一种含锌指的转录因子，但它在食管鳞状细胞癌（esophageal squamous cell carcinoma，ESCC）中潜在的调控机制仍不清楚。在这里，我们发现 KLF5 在 ESCC 中上调，其水平与肿瘤分化和淋巴结转移状态显著相关。上调的 KLF5 表达促进了 ESCC 细胞的增殖、迁移和侵袭。下调 KLF5 则表现出相反的效果。机制上，KLF5 通过上调成纤维细胞生长因子结合蛋白 1（fibroblast growth factor binding protein 1，FGF-BP1）和 SNAIL 家族转录抑制因子 2（snail family transcriptional repressor 2，SNAIL2）来发挥其肿瘤促进作用。KLF5 结合到 FGF-BP1 的启动子区域，并转录激活其表达。我们的研究表明，KLF5 可以通过上调 FGF-BP1/SNAIL2 信号通路来促进食管鳞癌细胞的增殖、迁移和侵袭。我们的工作表明，KLF5 可能是 ESCC 的原癌基因，并参与 ESCC 的转移。
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