LOXL1通过β-catenin-cyclinD介导的增殖促进胃癌进展。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research Pub Date : 2024-11-13 DOI:10.1016/j.yexcr.2024.114331

Jin-e Liang , Bo-wen Bao , Xue-hua He , Wen-qing Lu , Yang Liu , Jin Wang , Xiu-juan Qu , Dong-yang Li , Xiao-fang Che

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引用次数: 0

摘要

尽管晚期胃癌的化疗或靶向治疗取得了很大进展，但预后仍然很差。有必要筛选生物标志物来进行早期诊断和预后预测。然而，LOX 家族在胃癌中的预后价值以及促进胃癌进展的潜在分子机制仍不清楚。在 LOX 家族的五个成员中，LOXL1 是唯一的独立预后风险因子。根据LOXL1的表达和其他临床参数建立的提名图可以预测胃癌的总生存率。敲除（KD）LOXL1可减少胃癌细胞的增殖并导致G1期停滞。根据GSEA分析，LOXL1与WNT信号通路呈正相关，体外实验证明LOXL1-KD降低了β-catenin的磷酸化水平和下游G1期检查点CCND1的表达。

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LOXL1 promotes gastric cancer progression by β-catenin-cyclinD mediated proliferation

Although much progress has been made in chemotherapy or target therapy for advanced gastric cancer, the prognosis is still poor. It is necessary to screen biomarkers for early diagnosis and prognosis prediction. However, the prognostic value of LOX family in gastric cancer and the underlying molecular mechanisms for promoting the progression of gastric cancer remains unclear. Among five members of LOX family, LOXL1 was the unique independent prognostic risk factor. The nomogram established based on the expression of LOXL1 and other clinical parameters could predict the overall survival rate of gastric cancer. Knockdown (KD) of LOXL1 decreased cell proliferation and led to G1 phase arrest in gastric cells. According to GSEA analysis that LOXL1 was positively correlated with the WNT signaling pathway, in vitro experiment proved that LOXL1-KD reduced the phosphorylation level of β-catenin and the expression of the downstream G1 phase checkpoint CCND1. In conclusion, LOXL1 has been identified as a potential risk prognostic biomarker for gastric cancer by promoting gastric cancer proliferation via WNT/β-catenin/cyclinD1 pathway.

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来源期刊

Experimental cell research 医学-细胞生物学

CiteScore

7.20

自引率

0.00%

发文量

295

审稿时长

30 days

期刊介绍： Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.