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

Siyang Feng, Jianxue Zhai, Di Lu, Jie Lin, Xiaoying Dong, Xiguang Liu, Hua Wu, Anja Roden, Giovanni Brandi, Simona Tavolari, Andrea Bille, Kaican Cai

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
JournalExperimental Cell Research
DOIs
StateAccepted/In press - Jan 1 2018

Fingerprint

Claudin-1
Epithelial-Mesenchymal Transition
Non-Small Cell Lung Carcinoma
Growth
Neoplasms
Cell Line

Keywords

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

ASJC Scopus subject areas

  • Cell Biology

Cite this

TUSC3 accelerates cancer growth and induces epithelial-mesenchymal transition by upregulating claudin-1 in non-small-cell lung cancer cells. / Feng, Siyang; Zhai, Jianxue; Lu, Di; Lin, Jie; Dong, Xiaoying; Liu, Xiguang; Wu, Hua; Roden, Anja; Brandi, Giovanni; Tavolari, Simona; Bille, Andrea; Cai, Kaican.

In: Experimental Cell Research, 01.01.2018.

Research output: Contribution to journalArticle

Feng, Siyang ; Zhai, Jianxue ; Lu, Di ; Lin, Jie ; Dong, Xiaoying ; Liu, Xiguang ; Wu, Hua ; Roden, Anja ; Brandi, Giovanni ; Tavolari, Simona ; Bille, Andrea ; Cai, Kaican. / TUSC3 accelerates cancer growth and induces epithelial-mesenchymal transition by upregulating claudin-1 in non-small-cell lung cancer cells. In: Experimental Cell Research. 2018.
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AU - Lin, Jie

AU - Dong, Xiaoying

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AU - Wu, Hua

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AB - 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.

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