Fig. 4: HMGA1 promoted malignant phenotypes and chemoresistance of glioma cells via MYH9. | Cell Death & Disease

Fig. 4: HMGA1 promoted malignant phenotypes and chemoresistance of glioma cells via MYH9.

From: HMGA1 stimulates MYH9-dependent ubiquitination of GSK-3β via PI3K/Akt/c-Jun signaling to promote malignant progression and chemoresistance in gliomas

Fig. 4

A–C MTT (A and B) and Edu incorporation (C) assays showed that MYH9 upregulation reversed the shHMGA1-mediated reduction of growth ability in glioma cells. D, E Transwell (D) and Boyden (E) chamber assays verified that the ability of cell invasion and migration was recovered in shHMGA1+ MYH9 plasmid-treated cells group compared to shHMGA1-treated cells group. F, G Dose–response curves for TMZ showed the TMZ concentration causing IC50 was rescued in shHMGA1+MYH9 plasmid-treated cells groups compared to shHMGA1-treated cells groups. H Western blot assay confirmed MYH9 upregulation rescued shHMGA1-mediated reduction of the EMT-related proteins, the cell cycle-related factors, and the stemness-related factors, and MYH9-overexpression could reverse the shHMGA1-mediated increase of GSK-3β.

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