SFPQ Promotes Lung Cancer Malignancy via Regulation of CD44 v6 Expression

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.

Automated summary

This study identifies SFPQ as a key nuclear protein regulator that is overexpressed in lung cancer MSCs and promotes their proliferation, chemotherapy resistance, and invasion. Knockdown of SFPQ inhibits the stemness and proliferation of lung cancer MSCs in vitro, as well as metastasis in vivo. These findings suggest that SFPQ may serve as a potential therapeutic target for limiting growth, chemotherapy resistance, and metastasis of lung cancer.