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<p>Migration is a critical driver in the initiation and progression of gastric cancer. However, the involvement of RNA–RNA interactions in this process remains poorly understood. Previous work from our group and others has established RBP2 (RB-Binding Protein 2) and SOX4 (SRY-related high-mobility-group box 4) as key regulators of tumor development, influencing processes such as cell proliferation, differentiation, survival, and migration. Here, we demonstrate that RBP2 regulates SOX4 expression at both the mRNA and protein levels <i>via</i> a miRNA- and 3′UTR-dependent mechanism. Integrated bioinformatics and experimental analyses revealed downregulation of miR-212-3p and concomitant overexpression of RBP2 and SOX4 during gastric carcinogenesis. Importantly, miR-212-3p was identified as a shared upstream regulator of both RBP2 and SOX4. Knockdown of RBP2 consistently reduced SOX4 expression, supporting its role as a upstream regulator. Furthermore, we showed that the 3′UTR of RBP2 promotes gastric cancer cell migration by enhancing the expression of both RBP2 and SOX4. Collectively, our findings reveal the oncogenic function of the RBP2 3′UTR and delineate a novel RBP2–miR-212-3p–SOX4 regulatory axis, providing mechanistic insights with potential diagnostic and therapeutic relevance for gastric cancer.</p>

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RBP2 promotes gastric cancer cell migration by acting as a competitive endogenous RNA to upregulate SOX4 via sponging miR-212-3p

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月10日

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  • Liu Jilan,
  • Wang Haocheng,
  • Sun Kaiyue,
  • Li Xize,
  • Zeng Jiping

摘要

Migration is a critical driver in the initiation and progression of gastric cancer. However, the involvement of RNA–RNA interactions in this process remains poorly understood. Previous work from our group and others has established RBP2 (RB-Binding Protein 2) and SOX4 (SRY-related high-mobility-group box 4) as key regulators of tumor development, influencing processes such as cell proliferation, differentiation, survival, and migration. Here, we demonstrate that RBP2 regulates SOX4 expression at both the mRNA and protein levels via a miRNA- and 3′UTR-dependent mechanism. Integrated bioinformatics and experimental analyses revealed downregulation of miR-212-3p and concomitant overexpression of RBP2 and SOX4 during gastric carcinogenesis. Importantly, miR-212-3p was identified as a shared upstream regulator of both RBP2 and SOX4. Knockdown of RBP2 consistently reduced SOX4 expression, supporting its role as a upstream regulator. Furthermore, we showed that the 3′UTR of RBP2 promotes gastric cancer cell migration by enhancing the expression of both RBP2 and SOX4. Collectively, our findings reveal the oncogenic function of the RBP2 3′UTR and delineate a novel RBP2–miR-212-3p–SOX4 regulatory axis, providing mechanistic insights with potential diagnostic and therapeutic relevance for gastric cancer.