Research Papers:

Loss of Par3 promotes lung adenocarcinoma metastasis through 14-3-3ζ protein

Song Tong, Tian Xia, Kai Fan, Ke Jiang, Wei Zhai, Jing-Song Li, Si-Hua Wang _ and Jian-Jun Wang

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Oncotarget. 2016; 7:64260-64273. https://doi.org/10.18632/oncotarget.11728

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Song Tong1, Tian Xia1, Kai Fan1, Ke Jiang1, Wei Zhai1, Jing-Song Li1, Si-Hua Wang1, Jian-Jun Wang1

1Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

Correspondence to:

Si-Hua Wang, email: [email protected]

Jian-Jun Wang, email: [email protected]

Keywords: NSCLC, Par3, 14-3-3ζ, metastasis

Received: April 29, 2016     Accepted: August 13, 2016     Published: August 31, 2016


Partitioning defective protein 3 (Par3) can activate the Tiam1/Rac pathway to inhibit invasion and metastasis in many cancers; however, the role of Par3 in lung adenocarcinoma remains unknown. Here we show that Par3 is downregulated in lung adenocarcinoma tissues and is associated with higher rates of lymph node metastasis and recurrence. Our functional study demonstrated that knock-down of Par3 promoted lung adenocarcinoma cell growth, cell migration, tumor formation, and metastasis, all of which were effectively inhibited when 14-3-3ζ was silenced. We found that Par3 binded with 14-3-3ζ protein and also showed that Par3 abrogated the binding of 14-3-3ζ to Tiam1, which was responsible for Rac1 activation. Knock-down of 14-3-3ζ inhibited Tiam1/Rac-GTP activation and blocked the invasive behavior of cells lacking Par3. These data suggest that loss of Par3 promotes metastatic behavior in lung adenocarcinoma cells through 14-3-3ζ protein.

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