Fig. 5: CELF2 inhibited HCC cell proliferation, migration, and chemoresistance and was involved in CRNDE-mediated oncogenic effect. | Cell Death & Disease

Fig. 5: CELF2 inhibited HCC cell proliferation, migration, and chemoresistance and was involved in CRNDE-mediated oncogenic effect.

From: LncRNA CRNDE facilitates epigenetic suppression of CELF2 and LATS2 to promote proliferation, migration and chemoresistance in hepatocellular carcinoma

Fig. 5

a Relative expression of CELF2 in HCC tumor tissues and corresponding adjacent tissues was determined by qPCR (n = 47). b GEPIA was accessed and CELF2 expression in healthy human individual (n = 160) and in HCC patients (n = 369) was compared. c Expression of CELF2 was detected in HCCC-9810, Bel-100, Bel-7402, Bel-7405, HUH-7, SMMC-7721, HepG2, WRL68, and THLE3. d CELF2 was cloned into pcDNA3.1(+) and overexpressed in Bel-100 and Huh-7 cells. CELF2 expression was determined by WB and empty vectors were used as a negative control. e, f Cell vitality was evaluated by MTT assay in Bel-100 (e) and Huh-7 cells (f). g, h Cell migration and invasive abilities were determined by transwell assays in in Bel-100 (g) and Huh-7 cells (h). i Huh-7 and Huh-7/ADR cells were transfected with pcDNA3.1(+)-CELF2 or empty vectors, and relative cell viability was detected by MTT assay combined with ADR. j ADR IC50 was determined in both Huh-7 and Huh-7/ADR cells. k Bel-100 cell were transfected with shCRNDE alone or co-transfected with shCRNDE and siCELF2, cell viability was measured by MTT assay. l Transwell assay was used to determine the cell migration and invasive abilities in Bel-100 transfected with shCRNDE and/or siCELF2. The data were shown as mean ± SD based on at least three independent experiments. *P < 0.05, **P < 0.01, and ***P < 0.001.

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