J Cancer 2020; 11(17):5032-5041. doi:10.7150/jca.45494

Research Paper

Inward Tension of Talin and Integrin-related Osmotic Pressure are involved Synergetically in the Invasion and Metastasis of Non-small Cell Lung Cancer

Ying Song1, Chen Li2, Yahan Fu2, Qiu Xie2, Jun Guo2, Guangming Li3✉, Huiwen Wu4✉

1. Department of Respiratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, PR China.
2. School of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, PR China.
3. Department of Anesthesiology, Huaian First People's Hospital, Nanjing Medical University, Huaian 223001, PR China.
4. Laboratory Center for Basic Medical Sciences, Nanjing Medical University, Nanjing 211166, PR China.

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Citation:
Song Y, Li C, Fu Y, Xie Q, Guo J, Li G, Wu H. Inward Tension of Talin and Integrin-related Osmotic Pressure are involved Synergetically in the Invasion and Metastasis of Non-small Cell Lung Cancer. J Cancer 2020; 11(17):5032-5041. doi:10.7150/jca.45494. Available from https://www.jcancer.org/v11p5032.htm

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Abstract

The integrin receptor protein talin plays vital roles in intracellular chemical and mechanical activities, and it is implicated in the high invasion and poor prognosis of non-small cell lung cancer (NSCLC). To better understand the mechanism underlying the function of talin in NSCLC invasion and metastasis, a few newly designed tension probe based on Förster resonance energy transfer was used for real-time observation of tension changes in A549 cells. High NSCLC cell aggressiveness was found to be accompanied with inward talin and outward glial fibrillary acidic protein (GFAP) tensions, which are closely associated with microfilament (MF) force and intracellular osmotic potential. The increased osmotic pressure resulted from the production of intracellular protein nanoparticles and the related ion influx. Furthermore, integrin activation was found to adjust the talin and GFAP tensions. Disruption of the interaction between talin and MFs blocked the mechanical source of talin, reducing both talin tension and osmotic pressure and thus inhibiting NSCLC cell invasion and migration. Consequently, our study demonstrates that talin is involved in NSCLC invasion and migration via its inward tension and that the integrin pathway is correlated closely with protein-nanoparticle-induced outward osmotic pressure.

Keywords: integrin receptor, non-small cell lung cancer, invasion, metastasis