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Supplementary Material 1

Additional file 1: Figure S1. The mRNA and protein expression of SPOP/Caprin1 in prostate cancer cells. Figure S2. Validation of SPOP/Caprin1 knockout in C4–2 cells. Figure S3. The SBC motif in Caprin1 is a degron recognized by SPOP. Figure S4. SPOP-ΔNLS mutant is constitutively localized in cytoplasm as puncta and more potent in promote Caprin1 degradation than wildtype SPOP-WT. Figure S5. SPOP knockout enhanced AS-induced SGs assembly in C4–2 cells. Figure S6. SPOP knockout enhances, while Carpin1 knockout suppresses Docetaxel-induced stress granules assembly in C4–2 cells. Figure S7. SPOP had no impact on clotrimazole-induced SG assembly. Figure S8. SPOP is dispensable for stress-induced translational arrest. Figure S9. SPOP had no impact on P-bodies assembly. Figure S10. Knockout or overexpression of Caprin1 marginally affected the growth or migration, but significantly increased stress-induced cell death in C4–2 cells. Figure S11. Validation of anti-Caprin1 antibody for IHC through using parental and Caprin1 knockout cells.

Preeclampsia (PE) is a pregnancy-induced disorder characterized by the overproliferation of trophoblasts. Hydatidiform moles, which are associated with a high risk of developing PE, are characterized by the excessive proliferation of trophoblastic tissue. H19 is highly expressed in placental tissue; however, its biological function remains unclear. A fundamental modification of the H19 gene is DNA methylation, which typically occurs in CG-rich regions at the promoter or the first exon region. In this study, in order to investigate the DNA methylation pattern of the H19 exon 1 region in placental tissues and trophoblast cells, placental specimens were collected from women in the first trimester of pregrancy (FTP) and the third trimester of pregnancy (TTP), as well as from from women with severe preeclampsia (sPE). We found that the DNA methylation levels of H19 exon 1 were significantly higher in the tissues obtained from women in TTP than from those obtained from women in FFP. The methylation status of CpG 1 sites within exon 1 of H19 was markedly higher in the placental tissues obtained from women with sPE than in the tissues obtained from women in TTP. In addition, we used the human choriocarcinoma cell line, JEG-3, and treated the cells with the methylation inhibitor, 5-aza-2'-deoxycytidine (5-Aza‑Dc). Following treatment with 5-Aza-Dc, the methylation levels at this CpG site showed marked hypomethylation. In addtion, the cell proliferative, migratory and invasive capacities of the cells were remarkably inhibited. Our data suggest that hypermethylation at individual CpG sites within exon 1 of H19 may be involved in the dysfunction of trophoblasts and the pathogenesis of PE.

Additional file 2: Table S1. Primers, sequences of shRNAs and siRNAs, antibody and chemicals. Table S2. SPOP mutation status, Caprin1 IHC scores in 131 cases of prostate cancer specimens and the associated clinical information. Table S3. Primers, sequences of shRNAs and siRNAs, antibody and chemicals.

Additional file 2: Table S1. Primers, sequences of shRNAs and siRNAs, antibody and chemicals. Table S2. SPOP mutation status, Caprin1 IHC scores in 131 cases of prostate cancer specimens and the associated clinical information. Table S3. Primers, sequences of shRNAs and siRNAs, antibody and chemicals.