Research Papers:

The role of talin2 in breast cancer tumorigenesis and metastasis

Liqing Li, Xiang Li, Lei Qi, Piotr Rychahou, Naser Jafari and Cai Huang _

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Oncotarget. 2017; 8:106876-106887. https://doi.org/10.18632/oncotarget.22449

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Liqing Li1,*, Xiang Li1,*, Lei Qi1, Piotr Rychahou1, Naser Jafari1 and Cai Huang1,2

1Markey Cancer Center, University of Kentucky, Lexington, KY 40506, USA

2Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY 40506, USA

*These authors contributed equally to this work

Correspondence to:

Cai Huang, email: [email protected]

Keywords: talin2; cell migration; invasion; tumor growth; metastasis

Received: August 06, 2017     Accepted: October 25, 2017     Published: November 06, 2017


Recent studies show that talin2 has a higher affinity to β-integrin tails and is indispensable for traction force generation and cell invasion. However, its roles in cell migration, cancer cell metastasis and tumorigenesis remain to be determined. Here, we used MDA-MB-231 human breast cancer cells as a model to define the roles of talin2 in cell migration, invasion, metastasis and tumorigenesis. We show here that talin2 knockdown (KD) inhibited cell migration and focal adhesion dynamics, a key step in cell migration, and that talin2 knockout (KO) inhibited cell invasion and traction force generation, the latter is crucial for cell invasion. Re-expression of talin2WT in talin2-KO cells restored traction force generation and cell invasion, but that of talin2S339C, a β-integrin-binding deficient mutant, did not. Moreover, talin2 KO (or KD) suppressed tumorigenesis and metastasis in mouse xenograft models. However, surprisingly, re-expression of talin2WT in talin2-KO cells did not rescue tumorigenesis. Thus, talin2 is required for breast cancer cell migration, invasion, metastasis and tumorigenesis, although exogenous expression of high levels of talin2 could inhibit tumorigenesis.

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