4.6 Article

Ribosomal Protein L23 Drives the Metastasis of Hepatocellular Carcinoma via Upregulating MMP9

Journal

FRONTIERS IN ONCOLOGY
Volume 11, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2021.779748

Keywords

RPL23; HCC; metastasis; RNA stability; MMP9

Categories

Funding

  1. National Natural Science Foundation of China [81861168035, 81922011, 81871656, 31571210, 81802437]
  2. Postdoctoral Science Foundation of China [2020M683261]
  3. Creative Research Group of CQ University [CXQT19016]
  4. Chongqing Natural Science Foundation [cstc2018jcyjAX0114]

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The study identified RPL23 as a driver of tumor metastasis in HCC, with its depletion inhibiting cell proliferation, migration, invasion, and distant metastasis. Mechanistically, RPL23 positively regulated MMP9 expression by directly associating with its 3'UTR, suggesting it may be a potential therapeutic target for HCC tumorigenesis and metastasis.
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths globally. Tumor metastasis is one of the major causes of high mortality of HCC. Identifying underlying key factors contributing to invasion and metastasis is critical to understand the molecular mechanisms of HCC metastasis. Here, we identified RNA binding protein L23 (RPL23) as a tumor metastasis driver in HCC. RPL23 was significantly upregulated in HCC tissues compared to adjacent normal tissues, and closely related to poor clinical outcomes in HCC patients. RPL23 depletion inhibited HCC cell proliferation, migration and invasion, and distant metastasis. Mechanistically, RPL23 directly associated with 3'UTR of MMP9, therefore positively regulated MMP9 expression. In conclusion, we identified that RPL23 might play an important role in HCC metastasis in an MMP9-dependent manner and be a potential therapeutic target for HCC tumorigenesis and metastasis.

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