Research Paper Volume 12, Issue 24 pp 26236—26247
Exosomal linc-FAM138B from cancer cells alleviates hepatocellular carcinoma progression via regulating miR-765
- 1 General Surgery, Affiliated Hospital of YouJiang Medical University For Nationalities, Baise 533000, Guangxi, China
- 2 Gastrointestinal Medicine, Affiliated Hospital of YouJiang Medical University For Nationalities, Baise 533000, Guangxi, China
- 3 YouJiang Medical University For Nationalities, Baise 533000, Guangxi, China
Received: August 27, 2020 Accepted: November 8, 2020 Published: December 26, 2020https://doi.org/10.18632/aging.202430
How to Cite
Copyright: © 2020 Zhuo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Exosomes are small vesicles with a diameter of 30-150 nm secreted by cells, which can be used as signal carriers to transfer nucleic acids, proteins, lipids and other functional substances to the recipient cells and play a role in cell communication. Hepatocellular carcinoma is the fourth most common cause of cancer-related death worldwide. Studies have shown that long non-coding RNAs (lncRNAs) are involved in the development and progression of many types of tumors. Our present study found that linc-FAM138B was reduced in HCC tissues and cell lines, low expression of linc-FAM138B indicated a poor prognosis in HCC patients. Interestingly, linc-FAM138B could be packaged into cancer cells. And exo-FAM138B inhibited the proliferation, migration and invasion of HCC cells. Furthermore, linc-FAM138B sponged miR-765 levels. And exo-si-FAM138B promoted HCC progression, while deletion of miR-765 reversed the role of exo-si-FAM138B. In vivo tumorigenesis experiments showed that exo-FAM138B suppressed HCC growth via modulating miR-765. In conclusion, exo-linc-FAM138B secreted by cancer cells inhibited HCC development via targeting miR-765, which provided a new idea and perspective for in-depth understanding of the complex signal regulation in HCC process.