Research progress on the role of the Wnt signaling pathway in pituitary adenoma

Wang, Wencai; Ma, Luyao; Zhao, Yongqiang; Liu, Menghao; Ye, Wei; Li, Xianfeng

doi:10.3389/fendo.2023.1216817

Cited by 1 publication

(1 citation statement)

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“…Dysregulation of this pathway often arises from mutations in various components, particularly mutations or silencing of Wnt tumor suppressors, with mutations in β-catenin being the most commonly observed alterations in cancer [30]. Aberrant Wnt/β-catenin signaling is closely associated with the development of numerous tumors, including PitNETs [31]. Gaston-Massuet et al [32] found that the expression of mutated β-catenin leads to a significant increase in the total number and proliferative potential of pituitary progenitor/stem cells.…”

Section: Discussionmentioning

confidence: 99%

Lysine Methyltransferase 5A Promotes the Progression of Growth Hormone Pituitary Neuroendocrine Tumors through the Wnt/β-Catenin Signaling Pathway

Li,

Song,

Chen

et al. 2024

Neuroendocrinology

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Introduction: Growth hormone (GH) secreting pituitary adenoma is considered one of the most harmful types of Pituitary Neuroendocrine Tumors (PitNETs). Our previous research has found that high expression of Lysine Methyltransferase 5A (KMT5A) is closely related to the proliferation of PitNETs. The aim of this study was to investigate the role and molecular mechanism of KMT5A in the progression of GH PitNETs. Methods: Immunohistochemistry, qRT-PCR and Western blot (WB) were used to assess the expression levels of KMT5A in human normal pituitary and GH PitNETs, as well as in rat normal pituitary and GH3 cells. Additionally, we utilized RNA interference technology and treatment with a selective KMT5A inhibitor to decrease the expression of KMT5A in GH3 cells. CCK-8, EdU, Flow cytometry (FCM), clone formation, and WB assay were further employed to evaluate the impact of KMT5A on the proliferation of GH3 cells in vitro. A xenograft model was established to evaluate the role of KMT5A in GH PitNETs progression in vivo. Results: KMT5A was highly expressed in GH PitNETs and GH3 cells. Moreover, the reduction of KMT5A expression led to inhibited growth of GH PitNETs and increased apoptosis of tumor cells, as indicated by the findings from CCK-8, EdU, clone formation and FCM assays. Additionally, WB analysis identified the Wnt/β-catenin signaling pathway as a potential mechanism through which KMT5A promotes GH PitNETs progression. Conclusion: Our research suggests that KMT5A may facilitate the progression of GH PitNETs via the Wnt/β-catenin signaling pathway. Therefore, KMT5A may serve as a potential therapeutic target and molecular biomarker for GH PitNETs.

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Section: Discussionmentioning

confidence: 99%