GOLM1 modulates EGFR/RTK cell-surface recycling to drive hepatocellular carcinoma metastasis
Summary The mechanism of cancer metastasis remains poorly understood. Using gene profiling of hepatocellular carcinoma (HCC) tissues, we have identified GOLM1 as a leading gene relating to HCC metastasis. GOLM1 expression is correlated with early recurrence, metastasis, and poor survival of HCC pati...
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| Main Authors: | , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
25 August 2016
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| In: |
Cancer cell
Year: 2016, Volume: 30, Issue: 3, Pages: 444-458 |
| ISSN: | 1878-3686 |
| DOI: | 10.1016/j.ccell.2016.07.017 |
| Online Access: | Verlag, kostenfrei, Volltext: http://dx.doi.org/10.1016/j.ccell.2016.07.017 Verlag, kostenfrei, Volltext: http://www.sciencedirect.com/science/article/pii/S1535610816303518 
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| Author Notes: | Qing-Hai Ye, Wen-Wei Zhu, Ju-Bo Zhang, Yi Qin, Ming Lu, Guo-Ling Lin, Lei Guo, Bo Zhang, Zhen-Hai Lin, Stephanie Roessler, Marshonna Forgues, Hu-Liang Jia, Lu Lu, Xiao-Fei Zhang, Bao-Feng Lian, Lu Xie, Qiong-Zhu Dong, Zhao-You Tang, Xin Wei Wang, Lun-Xiu Qin |
| Summary: | Summary The mechanism of cancer metastasis remains poorly understood. Using gene profiling of hepatocellular carcinoma (HCC) tissues, we have identified GOLM1 as a leading gene relating to HCC metastasis. GOLM1 expression is correlated with early recurrence, metastasis, and poor survival of HCC patients. Both gain- and loss-of-function studies determine that GOLM1 acts as a key oncogene by promoting HCC growth and metastasis. It selectively interacts with epidermal growth factor receptor (EGFR) and serves as a specific cargo adaptor to assist EGFR/RTK anchoring on the trans-Golgi network (TGN) and recycling back to the plasma membrane, leading to prolonged activation of the downstream kinases. These findings reveal the functional role of GOLM1, a Golgi-related protein, in EGFR/RTK recycling and metastatic progression of HCC. |
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| Item Description: | Gesehen am 22.12.2017 |
| Physical Description: | Online Resource |
| ISSN: | 1878-3686 |
| DOI: | 10.1016/j.ccell.2016.07.017 |