ArticleMolecular biotechnology2024
miR-181-5p/KLHL5 Promoted Proliferation and Migration of Gastric Cancer Through Activating METTL3-Mediated m6A Process.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- RNF125 mediates the anti-breast cancer activity of betulinic acid through ubiquitin-dependent degradation of MYH9.International journal of clinical oncology · 2026Article
- Exosome-Transferred STAT3 from Cancer-Associated Fibroblasts Expedites Thymic Carcinoma Malignant Progression and M2 Macrophage Polarization Through Transcriptionally Activating KLHL5.Applied biochemistry and biotechnology · 2026Article
- From inflammation to carcinogenesis: MiRNA regulates epithelial-mesenchymal transition to facilitate malignant progression of gastric precancerous lesions.Frontiers in oncology · 2026Review
- Histone lactylation drives METTL3 upregulation-mediated RNA m6A modification of CCT2 to hinder CD8Cellular and molecular life sciences : CMLS · 2025Article
- METTL3-driven m⁶A epigenetics in gastric cancer: unveiling oncogenic networks and clinical translation from tumorigenesis to therapy resistance.Cell biology and toxicology · 2025Review
- METTL3-Regulated lncRNA SNHG7 Drives MNNG-Induced Epithelial-Mesenchymal Transition in Gastric Precancerous Lesions.Toxics · 2024Article
- METTL3 as a potential therapeutic target in gastric cancer.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
KLHL5 was a member of kelch-repeat protein family and was involved in the initiation of progression of a plethora of cancers. However, its specific role in gastric cancer was not explicitly illustrated. In this context, we aimed to investigate the biological role and mechanisms about KLHL5 in gastric cancer. qRT-PCR and western blot were used to investigate the expression of KLHL5 and EMT biomarkers. Wound healing assay, CCK-8, and Transwell assay were used to investigate the biological function of KLHL5. We found that KLHL5 was highly expressed in gastric cancer both in vivo and in vitro; besides, its high expression led to a shorter overall survival. Following statistical analysis showed that KLHL5 was associated with M stage. As for molecular experiments, we found that KLHL5 knockdown significantly reduced the proliferation, migration, and invasion ability of gastric cancer cell line MKN45 and SGC-7901. Furthermore, we found that miR-181-5p targeted KLHL5 to regulate m6A level through METTL3. In addition, KLHL5 knockdown could significantly reduce the lung metastasis rate in mice. In conclusion, we found that miR-181-5p/KLHL5 could promote the proliferation, migration, and invasion of gastric cancer by activating m6A process through regulating METTL3.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.