ArticleCell death discovery2023
LncRNA TIALD contributes to hepatocellular carcinoma metastasis via inducing AURKA lysosomal degradation.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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
13 citing papers in PubMed, 16 citations in OpenAlex.
- RBM15B-mediated m6A modification of FOXM1 activates the AURKA/TPX2 axis to promote epithelial-mesenchymal transition-driven endometrial cancer progression.Cell adhesion & migration · 2026Article
- The lncRNA-m6A axis in cancer: a bidirectional regulatory network in tumor progression and therapeutic resistance.Journal of translational medicine · 2026Review
- METTL16-mediated upregulation of LINC00665 inhibits the apoptosis of breast cancer via regulating miR-28-5p/GLG1 axis.Translational cancer research · 2026Article
- GATA2 promotes hepatitis B virus-associated hepatocellular carcinoma development by regulating AURKA.Archives of microbiology · 2026Article
- METTL16 in cancer: Roles and regulatory mechanisms.Genes & diseases · 2026Review
- The methyltransferase METTL16 in digestive system cancers: functions and mechanisms.Frontiers in oncology · 2026Review
- The impact of ribosome association on lncRNA stability: a new layer of post-transcriptional control?Biochemical Society transactions · 2025Review
- RNA methylation in hepatocellular carcinoma: from metabolic reprogramming and immune escape mechanisms to small molecule inhibitor development.Journal of translational medicine · 2025Review
- Key oncogenes and candidate drugs for hepatitis-B-driven hepatocellular carcinoma progression.Discover oncology · 2025Article
- Revealing the active ingredients and mechanisms of Xiatianwu against hepatocellular carcinoma: a study based on network pharmacology and bioinformatics.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Targeting AURKA with multifunctional nanoparticles in CRPC therapy.Journal of nanobiotechnology · 2024Article
- The ncRNA-AURKA Interaction in Hepatocellular Carcinoma: Insights into Oncogenic Pathways, Therapeutic Opportunities, and Future Challenges.Life (Basel, Switzerland) · 2024Review
- Multifaceted bioinformatic analysis of m6A-related ferroptosis and its link with gene signatures and tumour-infiltrating immune cells in gliomas.Journal of cellular and molecular medicine · 2024Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
The N6-methyladenosine (m6A) RNA methyltransferase METTL16 is an emerging player in RNA modification landscape and responsible for the deposition of m6A in a few transcripts. AURKA (aurora kinase A) has been confirmed as an oncogene in cancer development including hepatocellular carcinoma (HCC). Nevertheless, it remains unclear whether METTL16 mediated m6A modification of lncRNAs can regulate AURKA activation in cancer progression. Here we aimed to investigate the functional links between lncRNAs and the m6A modification in AURKA signaling and HCC progression. Here we show that LncRNA TIALD (transcript that induced AURKA Lysosomal degradation) was down-regulated in HCC tissues by METTL16 mediated m6A methylation to facilitate its RNA degradation, and correlates with poor prognosis. Functional assays reveal that TIALD inhibits HCC metastasis both in vitro and in vivo. Mechanistically, TIALD directly interacts with AURKA and facilitate its degradation through the lysosomal pathway to inhibited EMT and metastasis of HCC. AURKA's specific inhibitor alisertib exerts effective therapeutic effect on liver cancer with low TIALD expression, which might provide a new insight into HCC therapy. Our study uncovers a negative functional loop of METTL16-TIALD-AURKA axis, and identifies a new mechanism for METTL16 mediated m6A-induced decay of TIALD on AURKA signaling in HCC progression, which may provide potential prognostic and therapeutic targets for HCC.
Identifiers
What Socratic holds
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 Socratic graph.