Abstract
Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Here, we identified that increased miR-23a expression in HCC tissues was associated with worse survival. More importantly, we found that STAT5A was a target of miR-23a, whose levels significantly decreased in tumor tissues. Stable expression of STAT5A in Huh7 cells suppressed glucose metabolism and tumor growth. Finally, this study showed that increased miR-23a negatively regulated STAT5A, which further activated AKT signaling to enable rapid metabolism for accelerated tumor growth in HCC. Taken together, our results demonstrated that the miR-23a-STAT5A-AKT signaling pathway is critical to alter glucose metabolism in HCC and may offer new opportunities for effective therapy. © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.
| Original language | English |
|---|---|
| Pages (from-to) | 710-724 |
| Journal | Molecular Oncology |
| Volume | 15 |
| Issue number | 2 |
| Online published | 6 Nov 2020 |
| DOIs | |
| Publication status | Published - Feb 2021 |
| Externally published | Yes |
Funding
This work was supported by the Key Project of Natural Science Foundations of China (No:81730097), Shanghai Sailing Program (20YF1459700), and the Project of Natural Science Foundations of China (No:82072618).
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Research Keywords
- AKT
- glucose metabolism
- hepatocellular carcinoma
- miR-23a
- STAT5A
- tumor growth
Publisher's Copyright Statement
- This full text is made available under CC-BY 4.0. https://creativecommons.org/licenses/by/4.0/
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