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<p>Gastric cancer (GC) constitutes a malignant neoplasm with elevatedmortality and dismal prognosis, featuring insidious early manifestation, apropensity for recurrence and metastasis, and drug resistance. Hence, there is anexigency to explore novel therapeutic tactics for GC. The expression of Cyclin B2(CCNB2) is augmented in a multiplicity of human malignancies, nevertheless,investigations into the correlation between CCNB2 and GC are scarce. Our studyreveal that CCNB2 is highly expressed in human GC tissues and significantlycorrelates with unfavorable survival prognoses in GC patients. Functional gain andloss assays demonstrated that CCNB2 can potentiate the proliferation and migrationof GC cells both in vitro and in vivo, while its overexpression facilitates theepithelial-mesenchymal transition (EMT) process of GC cells. The outcomes of RNAsequencing imply that CCNB2 is implicated in the activation of the PI3K/AKTsignaling pathway. Moreover, overexpression of RHBDL2 can countervail the inhibitionof the EMT process and the PI3K/AKT signaling mediated by CCNB2 in GC cells. Thus,targeting this newly identified pathway might constitute a prospective therapeuticstrategy for GC.</p>

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RETRACTED ARTICLE: Knockdown of CCNB2 inhibits the tumorigenesis of gastric cancer by regulation of the PI3K/Akt pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月17日

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  • Ming Hu,
  • Pengxian Tao,
  • Yongfeng Wang,
  • Chengzhang Zhu,
  • Yuntao Ma,
  • Xiaolong Liu,
  • Hui Cai

摘要

Gastric cancer (GC) constitutes a malignant neoplasm with elevatedmortality and dismal prognosis, featuring insidious early manifestation, apropensity for recurrence and metastasis, and drug resistance. Hence, there is anexigency to explore novel therapeutic tactics for GC. The expression of Cyclin B2(CCNB2) is augmented in a multiplicity of human malignancies, nevertheless,investigations into the correlation between CCNB2 and GC are scarce. Our studyreveal that CCNB2 is highly expressed in human GC tissues and significantlycorrelates with unfavorable survival prognoses in GC patients. Functional gain andloss assays demonstrated that CCNB2 can potentiate the proliferation and migrationof GC cells both in vitro and in vivo, while its overexpression facilitates theepithelial-mesenchymal transition (EMT) process of GC cells. The outcomes of RNAsequencing imply that CCNB2 is implicated in the activation of the PI3K/AKTsignaling pathway. Moreover, overexpression of RHBDL2 can countervail the inhibitionof the EMT process and the PI3K/AKT signaling mediated by CCNB2 in GC cells. Thus,targeting this newly identified pathway might constitute a prospective therapeuticstrategy for GC.