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<p>Leucine-rich repeat-containing protein 59 (LRRC59) has been implicated in the pathogenesis of various human cancers, but its functional role and underlying molecular mechanisms in cervical carcinogenesis and progression remain unknown. In this study, LRRC59 expression was assessed in cervical cancer (CC) and normal cervical tissues using public databases and clinical specimens. Correlations between LRRC59 expression and clinical characteristics were analyzed using data from our institutional cohort and The Cancer Genome Atlas (TCGA). The functional effects of LRRC59 on CC cell proliferation, apoptosis, invasion, and migration were evaluated through in vitro assays and xenograft tumor models. Potential mechanisms were identified by integrated bioinformatics analysis and subsequently validated experimentally. LRRC59 was significantly upregulated in CC tissues, and elevated LRRC59 expression correlated with poor prognosis. Knockdown of LRRC59 suppressed CC cell proliferation, invasion, and migration, while promoting apoptosis. Mechanistically, LRRC59 knockdown downregulated total β-catenin, nuclear β-catenin, and the expression of downstream targets c-Myc and cyclin D1. Treatment with SKL2001, a Wnt/β-catenin pathway agonist, partially reversed the inhibitory effects of LRRC59 knockdown on proliferation, invasion, and migration, as well as its pro-apoptotic effect. Furthermore, LRRC59 knockdown led to reduced expression of Y-box binding protein 1 (YBX1). Collectively, these findings demonstrate that LRRC59 promotes CC progression likely via YBX1-mediated Wnt/β-catenin signaling, identifying LRRC59 as a promising prognostic biomarker and potential therapeutic target in cervical cancer.</p>

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Downregulation of LRRC59 suppresses cervical cancer progression likely by inhibiting YBX1-mediated Wnt/β-catenin signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月28日

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  • Qian Zhu,
  • Guiqin Xu,
  • Tianming Wang,
  • Zhuyun Ding,
  • Lianhua Liu,
  • Ling Ling,
  • Xiaoyan Ying

摘要

Leucine-rich repeat-containing protein 59 (LRRC59) has been implicated in the pathogenesis of various human cancers, but its functional role and underlying molecular mechanisms in cervical carcinogenesis and progression remain unknown. In this study, LRRC59 expression was assessed in cervical cancer (CC) and normal cervical tissues using public databases and clinical specimens. Correlations between LRRC59 expression and clinical characteristics were analyzed using data from our institutional cohort and The Cancer Genome Atlas (TCGA). The functional effects of LRRC59 on CC cell proliferation, apoptosis, invasion, and migration were evaluated through in vitro assays and xenograft tumor models. Potential mechanisms were identified by integrated bioinformatics analysis and subsequently validated experimentally. LRRC59 was significantly upregulated in CC tissues, and elevated LRRC59 expression correlated with poor prognosis. Knockdown of LRRC59 suppressed CC cell proliferation, invasion, and migration, while promoting apoptosis. Mechanistically, LRRC59 knockdown downregulated total β-catenin, nuclear β-catenin, and the expression of downstream targets c-Myc and cyclin D1. Treatment with SKL2001, a Wnt/β-catenin pathway agonist, partially reversed the inhibitory effects of LRRC59 knockdown on proliferation, invasion, and migration, as well as its pro-apoptotic effect. Furthermore, LRRC59 knockdown led to reduced expression of Y-box binding protein 1 (YBX1). Collectively, these findings demonstrate that LRRC59 promotes CC progression likely via YBX1-mediated Wnt/β-catenin signaling, identifying LRRC59 as a promising prognostic biomarker and potential therapeutic target in cervical cancer.