通过调节信号传导促进食管癌。
promotes esophageal carcinoma through regulating signaling.
作者信息
Tang Zhaohui, Jiang Yongjun, Zong Yuyu, Ding Sijuan, Wu Chen, Tang Zhangwen, Liao Lin, Jiang Shaohui, Tang Ruoting, Li Fang, Luo Pengfei
机构信息
Department of Oncology, The Central Hospital of Yongzhou, Hunan Province, Yongzhou, 425000, China.
出版信息
Epigenomics. 2024;16(17):1133-1148. doi: 10.1080/17501911.2024.2388018. Epub 2024 Sep 5.
To investigate function of somatostatin receptor 5 antisense RNA 1 (SSTR5-AS1) in esophageal carcinoma (ESCA). The cellular function was assessed using EdU staining and Transwell assay. The localization of SSTR5-AS1 was measured using fluorescence hybridization staining. shRNA repressed invasion and migration and induced apoptosis in ESCA cells. SSTR5-AS1 was distributed in cytoplasm, and it regulated its subunit integrin beta 6 (ITGB6) via eukaryotic translation initiation factor 4A3 (EIF4A3). SSTR5-AS1 shRNA inactivated ITGB6 and JAK1/STAT3 signaling. SSTR5-AS1 silencing attenuated the malignant behavior of ESCA cells through the ITGB6-mediated JAK1/STAT3 axis. SSTR5-AS1 promotes tumorigenesis of ESCA by interacting with EIF4A3 to regulate ITGB6/JAK1/STAT3 axis, which serves a basis for discovering strategies against ESCA.
研究生长抑素受体5反义RNA 1（SSTR5-AS1）在食管癌（ESCA）中的作用。采用EdU染色和Transwell实验评估细胞功能。使用荧光杂交染色检测SSTR5-AS1的定位。shRNA抑制ESCA细胞的侵袭和迁移并诱导其凋亡。SSTR5-AS1分布于细胞质中，并通过真核翻译起始因子4A3（EIF4A3）调节其亚基整合素β6（ITGB6）。SSTR5-AS1 shRNA使ITGB6和JAK1/STAT3信号失活。SSTR5-AS1沉默通过ITGB6介导的JAK1/STAT3轴减弱ESCA细胞的恶性行为。SSTR5-AS1通过与EIF4A3相互作用调节ITGB6/JAK1/STAT3轴促进ESCA的肿瘤发生，这为发现抗ESCA策略提供了依据。
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