Fig. 2: miR-17-5p promoted MM cell proliferation, colony formation, cell cycle progression, and inhibited cell apoptosis in vitro and in vivo. | Cell Death & Disease

Fig. 2: miR-17-5p promoted MM cell proliferation, colony formation, cell cycle progression, and inhibited cell apoptosis in vitro and in vivo.

From: Ferroportin downregulation promotes cell proliferation by modulating the Nrf2–miR-17-5p axis in multiple myeloma

Fig. 2

a The total RNA was isolated from ARP1 and OCI-MY5 cells and the level of miR-17-5p mRNA were determined by qRT-PCR after transfection of control and miR-17-5p mimic. Overexpression of miR-17-5p promoted cell proliferation b, colony formation c, cell cycle progression d, and inhibited apoptosis h, while miR-17-5p knockdown was assessed by qRT-PCR j and inhibited cell proliferation k, colony formation l, cell cycle progression m, and promoted apoptosis q in myeloma cells. Western blot analysis of cell-cycle regulator proteins Cyclin D1, CDK4, and CDK6 e, n, apoptosis-related protein expression i, r in the presence and absence of miR-17-5p. Representative pictures of MM xenografts from both ARP1-miR-17-5p f and ARP1-anti-miR-17-5p cells o. Tumor growth curve revealing that miR-17-5p overexpression significantly promotes growth g, while miR-17-5p knockdown inhibits tumor growth in vivo. *p < 0.05; **p < 0.01

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