Scholarlink

<p>Low-density lipoprotein receptor (LDLR)-related protein 6 (LRP6) has been found to be highly expressed in various solid tumors, correlating with malignant phenotypes and poor prognosis. However, the role of LRP6 in diffuse large B cell lymphoma (DLBCL) remains unclear. In this study, we revealed that LRP6 expression was significantly elevated in DLBCL patients. High expression of LRP6 is not only associated with tumor subtype, Ann Arbor stage, and extra-nodal invasion, but also with poor prognosis. The knockout of LRP6 significantly inhibited cell proliferation and migration, induced cell cycle arrest, and promoted apoptosis in DLBCL cells. Mechanistically, LRP6 knockout inhibited both the Wnt/β-catenin and mTORC1 signaling pathways. Furthermore, we found that LRP6 knockout reduced the expression of indoleamine 2,3-dioxygenase 1 (IDO1), a negative regulator within the tumor microenvironment (TME), and consequently decreased the level of kynurenine (KYN), indicating a reduction in IDO1 enzymatic activity. Additionally, LRP6 knockout suppressed DLBCL xenograft tumor growth. Collectively, our findings suggested that high LRP6 expression in DLBCL patients was associated with poor prognosis, and LRP6 contributes to DLBCL progression and immunosuppression. Taken together, these findings highlight LRP6 as a potential novel prognostic biomarker and therapeutic target.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

LRP6 aggravates proliferation, invasion, and immunosuppression in diffuse large B-cell lymphoma: a novel prognostic marker and therapy target

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月20日

查看全文
  • Liangliang Li,
  • Jincai Yang,
  • Huan Liu,
  • Lingling Yue,
  • Tingyong Cao,
  • Pengyun Zeng

摘要

Low-density lipoprotein receptor (LDLR)-related protein 6 (LRP6) has been found to be highly expressed in various solid tumors, correlating with malignant phenotypes and poor prognosis. However, the role of LRP6 in diffuse large B cell lymphoma (DLBCL) remains unclear. In this study, we revealed that LRP6 expression was significantly elevated in DLBCL patients. High expression of LRP6 is not only associated with tumor subtype, Ann Arbor stage, and extra-nodal invasion, but also with poor prognosis. The knockout of LRP6 significantly inhibited cell proliferation and migration, induced cell cycle arrest, and promoted apoptosis in DLBCL cells. Mechanistically, LRP6 knockout inhibited both the Wnt/β-catenin and mTORC1 signaling pathways. Furthermore, we found that LRP6 knockout reduced the expression of indoleamine 2,3-dioxygenase 1 (IDO1), a negative regulator within the tumor microenvironment (TME), and consequently decreased the level of kynurenine (KYN), indicating a reduction in IDO1 enzymatic activity. Additionally, LRP6 knockout suppressed DLBCL xenograft tumor growth. Collectively, our findings suggested that high LRP6 expression in DLBCL patients was associated with poor prognosis, and LRP6 contributes to DLBCL progression and immunosuppression. Taken together, these findings highlight LRP6 as a potential novel prognostic biomarker and therapeutic target.