细胞通过力学感受器接收外界物理力学信号，并由细胞骨架系统产生相对应的细胞内部物理力学系统和信号传递系统。细胞力学系统失调会导致包括肿瘤在内的多种疾病。我们的前期工作揭示了机械力传导通路的开关分子SWI/SNF调节YAP/TAZ 的活性，进而影响细胞的增殖和癌变。.以碳重离子放疗为代表的新型放射疗法在临床实践中取得了令人瞩目的成绩，然而其背后的生物学机制我们还不甚了解。在前期工作中我们发现了受碳重离子辐射诱导的LNC CRYBG3能够调控肌动蛋白组装，并且具有抑癌功能。结合前期工作我们提出：LNC CRYBG3是否作为连接电离辐射和生物力学传导通路的纽带，通过调节生物力学传导通路效应分子YAP/TAZ的活性来调控肿瘤的增殖和侵袭转移。据此，我们提出“电离辐射-->LNC CRYBG3 --|F-actin --|SWI/SNF --|YAP/TAZ-->肿瘤增殖、侵袭转移”调控机制的假说。

Cells receive multiple levels of mechanic force, from cell-cell contact level to tissue level. The receptor from cell membrane can pass this message though mechanotransduction pathways. It has been well recognized that miss regulation of mechanotransduction can cause many diseases or even cancer. Previously, we have reported that the SWI/SNF complex is a mechanoregulated inhibitor of YAP/TAZ. Mutation of SWI/SNF could disrupt mechanotransduction and induce cancer formation..On the other hand, it is remarkable that the radiation-therapy, especially by using heavy irons, have significant outcome from surgery of cancer therapy. As new generation of radiation-therapy, accelerated carbon beams have several advantages and better prognosis. But the mechanism is still mystery. In our previous research, we found a long non coding RNA (LNC CRYBG3) is induced by accelerated carbon beams. Overexpression of LNC CRYBG3 could block formation of F-actin, changing the cytoskeleton system. In vivo experiments, we fund that LNC CRYBG3 plays inhibitor role during cancer development. Then we asked, if it is possible that LNC CRYBG3 serves like a bridge link the iron radiation (IR) to mechanotransduction? Following this idea, we propose a new pathway : “IR-->LNC CRYBG3 --| F-actin --| SWI/SNF --| YAP/TAZ”.