Cai Ming, Liu Pengcheng, Wei Li, Wang Jinshen, Qi Jin, Feng Shengmei, Deng Lianfu
Shanghai Institute of Traumatology and Orthopaedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases with Integrated Chinese-Western Medicine, Ruijin Hospital, Jiao Tong University School of Medicine, Shanghai, China.
Department of Orthopaedics, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
PLoS One. 2014 Jan 15;9(1):e84833. doi: 10.1371/journal.pone.0084833. eCollection 2014.
Previous studies have shown that the rate of breast cancer metastasis correlates with the expression of vacuolar H(+)-ATPases (V-ATPases). However, how V-ATPase is involved in breast cancer metastasis remains unknown. Our previous study showed that Atp6v1c1-depleted osteoclasts did not form organized actin rings and that Atp6v1c1 co-localizes with F-actin. In this study, we found that the normal arrangement of filamentous actin is disrupted in Atp6v1c1-depleted 4T1 mouse breast cancer cells and in the ATP6V1C1-depleted human breast cancer cell lines MDA-MB-231 and MDA-MB-435s. We further found that Atp6v1c1 co-localizes with F-actin in 4T1 cells. The results of our study suggest that high expression of Atp6v1c1 affects the actin structure of cancer cells such that it facilitates breast cancer metastasis. The findings also indicate that Atp6v1c1 could be a novel target for breast cancer metastasis therapy.
先前的研究表明，乳腺癌转移率与液泡H(+)-ATP酶（V-ATP酶）的表达相关。然而，V-ATP酶如何参与乳腺癌转移仍不清楚。我们先前的研究表明，Atp6v1c1缺失的破骨细胞不会形成有组织的肌动蛋白环，且Atp6v1c1与F-肌动蛋白共定位。在本研究中，我们发现，在Atp6v1c1缺失的4T1小鼠乳腺癌细胞以及ATP6V1C1缺失的人乳腺癌细胞系MDA-MB-231和MDA-MB-435s中，丝状肌动蛋白的正常排列被破坏。我们进一步发现，Atp6v1c1在4T1细胞中与F-肌动蛋白共定位。我们的研究结果表明，Atp6v1c1的高表达会影响癌细胞的肌动蛋白结构，从而促进乳腺癌转移。这些发现还表明，Atp6v1c1可能是乳腺癌转移治疗的一个新靶点。
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