Journal
ISCIENCE
Volume 25, Issue 3, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2022.103984
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Funding
- Natural Science Foundation of Tianjin-Municipal Science and Technology Commission (CN) [20JCYBJC01030]
- Social Development Science and Technology Project of TaiZhou City [21ywb99]
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This study demonstrates the role of ALAHM in tumor-derived extracellular vesicles (EVs) in promoting liver metastasis of lung adenocarcinoma (LUAD) cells. ALAHM enhances the proliferation, invasion, and migration of LUAD cells, and induces hepatocyte secretion of HGF. The findings suggest that LUAD-cell-derived EVs containing ALAHM contribute to the progression of liver metastasis in LUAD.
Tumor-derived extracellular vesicles (EVs) are involved in tumor metastasis. Highly enriched IncRNA-ALAHM was identified from serum EVs of lung adenocarcinoma (LUAD) patients with liver metastasis by high-throughput sequencing. A mouse model of in situ lung cancer was used to determine the effect of ALAHM in LUAD cell EVs on liver metastasis. The effects of ALAHM on hepatocyte paracrine HGF as well as proliferation, invasion, and migration of LUAD cells were observed in vitro. As results, ALAHM expression in LUAD cell EVs was significantly increased. LUAD-cell-derived EVs overexpressing ALAHM significanly promoted lung cancer liver metastasis in model mice. ALAHM of LUAD cell EVs also promotes hepatocyte parasecretion of HGF by binding with AUF1 and increases the proliferation, invasion, and migration of LUAD cells. Thus, LUAD-cell-derived EVs containing ALAHM causes increasing HGF and promoting liver metastasis of LUAD cells.
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