SFPQ Promotes Lung Cancer Malignancy via Regulation of CD44 v6 Expression

被引:8
作者
Yang, Libang [1 ]
Yang, Jianbo [2 ,3 ]
Jacobson, Blake [4 ]
Gilbertsen, Adam [1 ]
Smith, Karen [1 ]
Higgins, LeeAnn [5 ]
Guerrero, Candace [5 ]
Xia, Hong [1 ]
Henke, Craig A. [1 ]
Lin, Jizhen [3 ,6 ]
机构
[1] Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA
[2] Univ Minneapolis, Sch Med, Dept Lab Med & Pathol, Minneapolis, MN USA
[3] Fujian Med Univ Union Hosp, Canc Ctr, Fuzhou, Peoples R China
[4] Univ Minnesota, Sch Med, Hematol Oncol & Transplantat, Minneapolis, MN USA
[5] Univ Minnesota, Ctr Mass Spectrometry & Prote, St Paul, MN USA
[6] Univ Minnesota, Canc Ctr, Dept Otolaryngol, Immunotherapy Res Lab, Minneapolis, MN 55455 USA
基金
美国国家卫生研究院;
关键词
mesenchymal stem cells (MSCs); lung non-small cell (NSC) cancer; nuclear fraction; quantitative proteomics; ingenuity pathway analysis; SFPQ; CD44v6; COLORECTAL-CANCER; TUMOR PROGRESSION; CELLS; PROTEOMICS; PROTEINS; IDENTIFICATION; METASTASIS; INVASION; BINDING; MIGRATION;
D O I
10.3389/fonc.2022.862250
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Mesenchymal stem cells (MSCs) contribute to tumor pathogenesis and elicit antitumor immune responses in tumor microenvironments. Nuclear proteins might be the main players in these processes. In the current study, combining spatial proteomics with ingenuity pathway analysis (IPA) in lung non-small cell (NSC) cancer MSCs, we identify a key nuclear protein regulator, SFPQ (Splicing Factor Proline and Glutamine Rich), which is overexpressed in lung cancer MSCs and functions to promote MSCs proliferation, chemical resistance, and invasion. Mechanistically, the knockdown of SFPQ reduces CD44v6 expression to inhibit lung cancer MSCs stemness, proliferation in vitro, and metastasis in vivo. The data indicates that SFPQ may be a potential therapeutic target for limiting growth, chemotherapy resistance, and metastasis of lung cancer.
引用
收藏
页数:13
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