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Exp Cell Res. 2018 Dec 15;373(1-2):44-56. doi: 10.1016/j.yexcr.2018.08.012. Epub 2018 Aug 9.

TUSC3 accelerates cancer growth and induces epithelial-mesenchymal transition by upregulating claudin-1 in non-small-cell lung cancer cells.

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Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, PR China.
Department of Pathology, Nanfang Hospital & School of Basic Medicine, Southern Medical University, 1838 Guangzhou Avenue, Guangzhou 510515, PR China.
Department of Laboratory Medicine and Pathology, Mayo Clinic Rochester, MN, USA.
Department of Experimental, Diagnostic and Specialty Medicine, University Hospital S. Orsola, Malpighi Bologna, via Massarenti 9, 40138, Italy.
Department of Thoracic Surgery, Guy's Hospital, London, UK.
Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, PR China. Electronic address:


Lung cancer is the most frequent cause of cancer-related deaths worldwide, but its molecular pathogenesis is poorly understood. The tumor suppressor candidate 3 (TUSC3) gene is located on chromosome 8p22 and is universally acknowledged as a cancer suppressor. However, our research has demonstrated that TUSC3 expression is significantly upregulated in non-small-cell lung cancer compared to benign controls. In this study, we analyzed the consequences of TUSC3 knockdown or overexpression on the biological functions of non-small-cell lung cancer cell lines. To identify the molecules and signaling pathways with which TUSC3 might interact, we completed immunoblotting, quantitative polymerase chain reaction, microarray, co-immunoprecipitation, and immunofluorescence assays. We demonstrated that TUSC3 knockdown leads to decreased proliferation, migration, and invasion, and reduced xenograft tumor growth of non-small-cell lung cancer cell lines, whereas opposite results were observed with overexpression of TUSC3. In addition, TUSC3 knockdown suppressed epithelial-mesenchymal transition by downregulating the expression of claudin-1, which plays an indispensable role in EMT progress. On the contrary, overexpression of TUSC3 significantly enhanced EMT progress by upregulating claudin-1 expression. Overall, our observations suggest that TUSC3 accelerates cancer growth and induces the epithelial-mesenchymal transition in non-small-cell lung cancer cells; we also identified claudin-1 as a target of TUSC3.


Claudin-1; EMT; Non-small-cell lung cancer; TUSC3

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