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<p>FOXO3 has been confirmed to be closely involved in the occurrence and progression of prostate cancer. In this study, we aimed to investigate the potential mechanisms of FOXO3 in prostate cancer progression. The expression of LINC00222 and FOXO3 in non-cancerous tissues and cancer tissues was detected by RT-qPCR. LINC00222 roles in regulating cell function in vitro as well as tumorigenesis in vivo were detected by gain-of-function and loss-of-function assays. The key protein expression was detected by western blotting assay. Dual luciferase reporter assay, bioinformatics analysis and immunoprecipitation assay were used to analyze the relationship between LINC00222 and miR-19a, miR-19a and FOXO3, or FOXO3 and APC. The results showed that the expression levels of both LINC00222 and FOXO3 were downregulated in prostate cancer tissues. In PC-3 cells, upregulation of FOXO3 significantly inhibited vimentin expression and promoted E-cadherin expression, as well as enhanced cell sensitivity to docetaxel. Compared to the control group, upregulation of LINC00222 in prostate cancer significantly inhibited cell proliferation and metastasis, and promoted cell apoptosis. Furthermore, LINC00222 competitively bound to miR-19a, enhanced FOXO3 expression, and then increased APC expression and inhibited the β-catenin signaling. Consistently, the in vivo experiments further confirmed the cancer inhibitory role of LINC00222 in prostate cancer. The present study revealed that LINC00222 adsorbed miR-19a to modulate FOXO3/APC/β-catenin signaling cascades and thereafter inhibited prostate cancer progression, which provided valuable insights into prostate cancer treatment.</p>

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LINC00222 regulates FOXO3 to interfere with β-catenin signaling pathway and suppresses prostate cancer progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月18日

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  • Hui Li,
  • Wenfeng Zhao,
  • Yuyou Deng,
  • Zhongcheng Liu,
  • Jiameng Li,
  • Shuoqi Tian

摘要

FOXO3 has been confirmed to be closely involved in the occurrence and progression of prostate cancer. In this study, we aimed to investigate the potential mechanisms of FOXO3 in prostate cancer progression. The expression of LINC00222 and FOXO3 in non-cancerous tissues and cancer tissues was detected by RT-qPCR. LINC00222 roles in regulating cell function in vitro as well as tumorigenesis in vivo were detected by gain-of-function and loss-of-function assays. The key protein expression was detected by western blotting assay. Dual luciferase reporter assay, bioinformatics analysis and immunoprecipitation assay were used to analyze the relationship between LINC00222 and miR-19a, miR-19a and FOXO3, or FOXO3 and APC. The results showed that the expression levels of both LINC00222 and FOXO3 were downregulated in prostate cancer tissues. In PC-3 cells, upregulation of FOXO3 significantly inhibited vimentin expression and promoted E-cadherin expression, as well as enhanced cell sensitivity to docetaxel. Compared to the control group, upregulation of LINC00222 in prostate cancer significantly inhibited cell proliferation and metastasis, and promoted cell apoptosis. Furthermore, LINC00222 competitively bound to miR-19a, enhanced FOXO3 expression, and then increased APC expression and inhibited the β-catenin signaling. Consistently, the in vivo experiments further confirmed the cancer inhibitory role of LINC00222 in prostate cancer. The present study revealed that LINC00222 adsorbed miR-19a to modulate FOXO3/APC/β-catenin signaling cascades and thereafter inhibited prostate cancer progression, which provided valuable insights into prostate cancer treatment.