Hefei Institutes of Physical Science
Chinese Academy of Sciences
Research News
Scientists Deepen Understanding on Oxygen-poor Zone in Liver Cancer
Date: 2018/07/04 Author: CHEN Xueran

A study team with Hefei Institutes of Physical Science made new discovery in oxygen-poor zone in liver cancer, shedding new light on liver cancer treatment.

This work was published last week in Journal of Experimental & Clinical Cancer Research.

Liver cancer is one of the most common malignant tumors in the world and its metastasis is the leading cause of associated death.

In that situation, there exists a special oxygen-poor zone near the center of cancer, which is caused by the short blood supply due to rapid growth of tumor cells.

Study shows that the situation of oxygen-poor could accelerate aggression of cancer cells and as ar result increase its metastatic risk. And worsely, it presents treatment resistance which makes it difficult to kill cancer cells in the clinical.

In this work, the team took a closer look at the special oxygen-poor zone, in which they found a new response factor, namely SVIL and its role in stress response.

Further, they observed a dramatic increase of SVIL in cancer cells compared with normal organs.

And in the situation of oxygen-poor, concentration of SVIL varied with the time of oxygen-poor.

Moreover, SVIL promoted epithelial-mesenchymal transition and metastasis of liver cancer cells in oxygen-poor situation via activation of the RhoA/ROCK-ERK/p38 pathway

The study result may highlight SVIL as a valuable prognostic biomarker and a potential therapeutic target in liver cancer cells.

This work was supported by grants from the National Natural Science Foundation of China, Anhui Provincial Nature Science Foundation and Youth Innovation Promotion Association of Chinese Academy of Sciences.

Link to the paper: Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway

Figure. Expression of supervillin in HCC enhances tumor metastasis in vivo. A, Bioluminescence imaging of representative mice at the end of the experiment. B, IHC staining showing the accumulation of HIF1α in mice with hepatic artery ligation (HAL), compared with those without HAL. C, Hematoxylin/eosin staining of lung tissues. Arrows indicate the metastatic tumor foci in the lung tissues. D, A schematic diagram showing the signaling axis of supervillin-RhoA/ROCK-ERK/p38 in HCC. Under hypoxia, supervillin levels increase and lead to RhoA activation. Activated RhoA regulates actin polymerization, induces the ROCK-ERK/p38 signaling pathway, and EMT, thereby promoting HCC cell migration, invasiveness, and metastasis.  (Image by CHEN Xueran)




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