Cheng Lina, Wang Hongwei, Han Shuangyin
Department of Gastroenterology, People's Hospital of Zhengzhou University (Henan Provincial People's Hospital), 7th Weiwu Road, Zhengzhou, 450003, Henan Province, China.
Department of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
Dig Dis Sci. 2017 Oct;62(10):2812-2820. doi: 10.1007/s10620-017-4670-3. Epub 2017 Aug 19.
Previous studies have reported that specific depletion of mammalian sterile-like kinase (MST1) in the mouse liver driven Hepatocellular carcinoma (HCC). However, how the expression of MST1 was regulated in the progression of HCC remains largely unknown.
The expression of miR-3910 in the HCC tissues and cell lines were examined using q-PCR. The functions of miR-3910 in HCC were examined using MTT assay, Boyden chamber assay and soft agar assay. The effects of miR-3910 on the metastasis of HCC cells were evaluated using the mouse model.
Here, we have shown that miR-3910 regulated the expression of MST1. MiR-3910 was up-regulated in HCC samples and cell lines, and the expression of miR-3910 was induced by the oncogenic RasV12. In the functional study, miR-3910 was found to promote the growth and migration of HCC cells, and knocking down miR-3910 inhibited the metastasis of HCC cells. Mechanically, it was found that miR-3910 activated YAP signaling by targeting MST1.
Taken together, this study demonstrated that miR-3910 exerted oncogenic effects on the progression of HCC and suggested that miR-3910 might be a therapeutic target for cancer therapy.
先前的研究报道，小鼠肝脏中哺乳动物不育样激酶（MST1）的特异性缺失会引发肝细胞癌（HCC）。然而，在HCC进展过程中MST1的表达是如何调控的，目前仍 largely unknown。
采用q-PCR检测HCC组织和细胞系中miR-3910的表达。使用MTT法、Boyden小室法和软琼脂法检测miR-3910在HCC中的功能。利用小鼠模型评估miR-3910对HCC细胞转移的影响。
在此，我们表明miR-3910调控MST1的表达。miR-3910在HCC样本和细胞系中上调，且miR-3910的表达由致癌性RasV12诱导。在功能研究中，发现miR-3910促进HCC细胞的生长和迁移，敲低miR-3910可抑制HCC细胞的转移。机制上，发现miR-3910通过靶向MST1激活YAP信号通路。
综上所述，本研究表明miR-3910对HCC的进展发挥致癌作用，并提示miR-3910可能是癌症治疗的一个治疗靶点。
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