ArticleDiscover oncology2025
LncRNA MSTO2P affects the proliferation, invasion and migration of non-small cell lung cancer by regulating the Wnt/β-catenin pathway.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Research progress on long non‑coding RNAs in lung cancer (Review).Molecular medicine reports · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
This study aimed to investigate the regulatory effects of the long non-coding RNA (lncRNA) MISATO family member 2 (MSTO2P) on non-small cell lung cancer (NSCLC) cell viability, invasion, and migration, as well as the underlying mechanism. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze the expression levels of MSTO2P. The effects of MSTO2P on cell viability, invasion, and migration were assessed using cell counting kit-8 (CCK-8), Transwell invasion, and wound healing assays in A549 and H1229 cells. A human phospho-kinase array kit was employed to identify potential phosphorylated kinases or signaling nodes affected by MSTO2P. The interaction between MSTO2P and β-catenin was evaluated using RNA pull-down and RNA immunoprecipitation (RIP) assays. A xenograft tumor mouse model was established to evaluate tumor growth. The results demonstrated that MSTO2P expression was elevated in NSCLC tissues and cells compared to normal counterparts. Silencing MSTO2P inhibited the viability, invasion, and migration of A549 and H1229 cells. MSTO2P interacted with β-catenin, thereby activating the Wnt/β-catenin pathway. Overexpression of MSTO2P or β-catenin promoted the viability, invasion, and migration of A549 and H1229 cells, effects that were reversed by treatment with XAV-939. In vivo studies showed that silencing MSTO2P suppressed tumor growth. In conclusion, MSTO2P promoted NSCLC cell viability, invasion, and migration by regulating the Wnt/β-catenin pathway, suggesting that MSTO2P may be a potential therapeutic target for NSCLC.
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