BMC medical genomics · 2026
HMGA1 promotes the proliferation, migration, and invasion of uveal melanoma cells via the PI3K/Akt/MMP-9 pathway.
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Ren Wanying, Luo Binhua
Аннотация
BACKGROUND: Uveal melanoma (UM) was prone to metastasis and had an extremely poor prognosis. High-mobility group protein A1 (HMGA1) was known to promote proliferation and invasion in various tumors, but its molecular mechanism in UM remained unclear.
OBJECTIVE: The effect of HMGA1 on the proliferation, migration, and invasion of UM cells was investigated, and whether it functioned through the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/matrix metalloproteinase-9 (MMP-9) pathway was explored.
METHODS: HMGA1 overexpression (OE) and knockdown (KD) models were established in two UM cell lines (C918, MUM-2B). Cell functions were assessed using MTT assay, EdU (5‑ethynyl‑2'‑deoxyuridine) incorporation assay, scratch wound healing assay, and Matrigel-Transwell assay. The expression of PI3K, phosphorylated PI3K (p-PI3K), Akt, phosphorylated Akt (p-Akt), and MMP-9 was detected by Western blot (WB). Pathway intervention was performed using the PI3K inhibitor LY294002.
RESULTS: Compared with the control group, HMGA1 overexpression significantly up-regulated the proliferation, migration, and invasion abilities of both cell lines, and led to a fold-dependent up-regulation of PI3K/Akt pathway activation and MMP-9 expression. In contrast, HMGA1 knockdown significantly down-regulated the above indicators. After treatment with LY294002, the tumor-promoting effects induced by HMGA1 overexpression were significantly reversed.
CONCLUSION: HMGA1 significantly promoted the proliferation, migration, and invasion of UM cells from different origins (primary C918, metastatic MUM-2B) by activating the PI3K/Akt pathway and upregulating MMP-9 expression, suggesting its potential as a target for molecular targeted therapy in UM.
OBJECTIVE: The effect of HMGA1 on the proliferation, migration, and invasion of UM cells was investigated, and whether it functioned through the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/matrix metalloproteinase-9 (MMP-9) pathway was explored.
METHODS: HMGA1 overexpression (OE) and knockdown (KD) models were established in two UM cell lines (C918, MUM-2B). Cell functions were assessed using MTT assay, EdU (5‑ethynyl‑2'‑deoxyuridine) incorporation assay, scratch wound healing assay, and Matrigel-Transwell assay. The expression of PI3K, phosphorylated PI3K (p-PI3K), Akt, phosphorylated Akt (p-Akt), and MMP-9 was detected by Western blot (WB). Pathway intervention was performed using the PI3K inhibitor LY294002.
RESULTS: Compared with the control group, HMGA1 overexpression significantly up-regulated the proliferation, migration, and invasion abilities of both cell lines, and led to a fold-dependent up-regulation of PI3K/Akt pathway activation and MMP-9 expression. In contrast, HMGA1 knockdown significantly down-regulated the above indicators. After treatment with LY294002, the tumor-promoting effects induced by HMGA1 overexpression were significantly reversed.
CONCLUSION: HMGA1 significantly promoted the proliferation, migration, and invasion of UM cells from different origins (primary C918, metastatic MUM-2B) by activating the PI3K/Akt pathway and upregulating MMP-9 expression, suggesting its potential as a target for molecular targeted therapy in UM.