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A number of genes involved in zygotic genome activation (ZGA) have been identified, but the RNA‐binding maternal factors that are directly related to ZGA in mice remain unclear. The present study shows that maternal deletion of Igf  2bp2 (also commonly known as Imp2 ) in mouse embryos causes early embryonic developmental arrest in vitro at the 2‐cell‐stage. Transcriptomics and proteomics analyses of 2‐cell‐stage embryos in mice reveal that deletion of IMP2 downregulates the expression of Ccar1 and Rps14 , both of which are required for early embryonic developmental competence. IGF2, a target of IMP2, when added in culture media, increases the proportion of wild‐type embryos that develop successfully to the blastocyst stage: from 29% in untreated controls to 65% (50 × 10 −9 m IGF2). Furthermore, in an experiment related to embryo transfer, foster mothers receiving IGF2‐treated embryos deliver more pups per female than females who receive untreated control embryos. In clinically derived human oocytes, the addition of IGF2 to the culture media significantly enhances the proportion of embryos that develop successfully. Collectively, the findings demonstrate that IMP2 is essential for the regulation and activation of genes known to be involved in ZGA and reveal the potential embryonic development‐related utility of IGF2 for animal biotechnology and for assisted reproduction in humans.

Background miR‐148‐3p and miR‐152‐3p as the tumor suppressors have been reported in various cancer types. Our study is aimed to discuss the synergistic effect of miR‐148‐3p and miR‐152‐3p in prostate cancer (PCa). Methods Bioinformatics algorithm and luciferase reporter assays were used to verify whether miR‐148‐3p and 152‐3p could bind with the 3′‐untranslated region (3′‐UTR) of Kruppel‐like factor 4 (KLF4). PCa cell growth in vivo was analyzed using the mouse xenograft tumor model. Results miR‐148‐3p and miR‐152‐3p were reduced in PCa tumor tissues. Moreover, the protein expression of KLF4 was increased in PCa tissues. The 3′‐UTR of KLF4 contained the conserved binding sites with miR‐148‐3p and miR‐152‐3p. The mimics or inhibitors of miR‐148‐3p and/or miR‐152‐3p could downregulated or upregulated KLF4 expression, respectively. miR‐148‐3p and miR‐152‐3p‐induced PCa cell growth inhibition were observed both in vivo and in vitro. KLF4 overexpression had the ability to neutralize the antitumor effect of miR‐148‐3p/152‐3p in vivo and in vitro. Conclusion miR‐148‐3p/152‐3p family could serve as tumor suppressors in PCa via repressing KLF4.