SESN1, negatively regulated by miR-377-3p, suppresses invasive growth of head and neck squamous cell carcinoma by interaction with SMAD3
SESN1, negatively regulated by miR-377-3p, suppresses invasive growth of head and neck squamous cell carcinoma by interaction with SMAD3
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SESN1 受 miR-377-3p 负调控，通过与 SMAD3 相互作用抑制头颈鳞状细胞癌的侵袭性生长
DOI：
10.1007/s13577-022-00719-z
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发表时间：
2022-05
期刊：
影响因子：
4.3
通讯作者：
Xia Juan
中科院分区：
文献类型：
--
作者：
Zhang Chi;Ren Lin;Zhang Hongjian;Yang Shiwen;Deng Miao;He Lihong;Cao Ruoyan;Zhao Chuanjiang;Xia Juan
Sestrin 1 （SESN1）是一种应激诱导蛋白，在许多癌症中抑制肿瘤。然而，SESN1在头颈部鳞状细胞癌（HNSCC）中的功能尚不清楚，需要进一步阐明。SESN1在HNSCC组织和细胞系中表达下调，SESN1低表达与HNSCC患者预后不良呈正相关。此外，SESN1过表达抑制HSC-6和CAL-33细胞的增殖、迁移和侵袭。此外，通过荧光素酶报告基因和RNA免疫沉淀实验证实了miR-377-3p与SESN1的结合关系。SESN1表达的下调与HNSCC组织中miR-377-3p的高水平一致。临床HNSCC组织线性回归分析显示miR-377-3p与SESN1表达呈负相关。此外，共免疫沉淀质谱分析显示，SESN1与SMAD3相互作用，SMAD3逆转了SESN1敲低引起的HSC-6和CAL-33细胞增殖、迁移和侵袭的增加。总之，这些发现提供了SESN1作为肿瘤抑制因子的证据，并揭示了miR-377-3p-SESN1-SMAD3调控轴在HNSCC发展过程中促进增殖、迁移和侵袭，这可能是HNSCC治疗的介入靶点。
Sestrin 1 (SESN1) is a stress-inducible protein that suppresses tumors in numerous cancers. However, the function of SESN1 in head and neck squamous cell carcinoma (HNSCC) is not clear and needs to be elucidated. Here, SESN1 expression was downregulated in HNSCC tissues and cell lines, and low SESN1 expression was positively correlated with poor prognosis in patients with HNSCC. Moreover, SESN1 overexpression inhibited the proliferation, migration, and invasion of HSC-6 and CAL-33 cells. In addition, the binding relationship between miR-377-3p and SESN1 was confirmed using luciferase reporter and RNA immunoprecipitation assays. Downregulation of SESN1 expression was consistent with high levels of miR-377-3p in HNSCC tissues. Linear regression analysis of clinical HNSCC tissues revealed a negative correlation between miR-377-3p and SESN1 expression. Moreover, co-immunoprecipitation mass spectrometry analysis revealed that SESN1 interacted with SMAD3, and SMAD3 reversed the increased proliferation, migration, and invasion of HSC-6 and CAL-33 cells caused by SESN1 knockdown. In conclusion, these findings provide evidence that SESN1 functions as a tumor suppressor and reveal the miR-377-3p-SESN1-SMAD3 regulatory axis that contributes to proliferation, migration, and invasion in HNSCC development, which may represent an interventional target for HNSCC therapy.
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