Fig. 3: Reduction in EPLIN expression promotes cancer cell growth and is associated with poorer overall survival. | Cell Death & Disease

Fig. 3: Reduction in EPLIN expression promotes cancer cell growth and is associated with poorer overall survival.

From: Identification of a small molecule targeting EPLIN as a novel strategy for the treatment of pediatric neuroblastoma and medulloblastoma

Fig. 3

A Illustration displaying the proteins in direct interaction with EPLIN in various key cellular biological functions. The data resource originally came from studies [25, 29]. B The top five significantly Up- and downregulated hallmark pathways in the EPLIN KO groups. The full list of altered hallmark pathways with significance can be found in Supplementary Table 4. C The expression levels of EPLIN in various cancer cell types and noncancer cells were analyzed using publicly available data from the Protein Atlas Cohort. D Immunoblots detecting EPLIN in immortalized hTERT RPE-1 and various neuroblastoma cells. Actin is loading control. E The overall survival rates of neuroblastoma patients with high and low EPLIN gene expression (the first quartile vs. the last quartile) were examined using Kaplan-Meier survival curves in SEQC498 (p = 0.0260), Cangelosi-786 (p = 0.0007), and Bell-97 datasets (p = 0.0087), which include 498, 786, and 97 neuroblastoma samples, respectively. Statistical analyses were conducted using the log-rank test, with data sourced from publicly available patient cohorts on the R2 microarray analysis and visualization platform. F The expression levels of EPLIN in IMR-32 parental and KO clones. Actin is loading control. G Response of IMR-32 parental, KO1, and KO2 clones to the indicated concentrations of FLIX5 for 72 h. One representative experiment with 3 technical replicates is shown (mean ± SD, t test, p < 0.05 is considered significant).

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