ArticleJournal of Cancer2017
Tat-interactive Protein-60KDA (TIP60) Regulates the Tumorigenesis of Lung Cancer In Vitro.
Article in Journal of Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 13 citations in OpenAlex.
- A narrative review of epigenetic marker in H3K27ac and its emerging potential as a therapeutic target in cancer.Epigenomics · 2025Review
- The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses.International journal of molecular sciences · 2024Review
- TIP60 is required for tumorigenesis in non-small cell lung cancer.Cancer science · 2023Article
- JAZF1: A metabolic actor subunit of the NuA4/TIP60 chromatin modifying complex.Frontiers in cell and developmental biology · 2023Review
- Insights into Regulators of p53 Acetylation.Cells · 2022Review
- Review
- Stabilization of the histone acetyltransferase Tip60 by deubiquitinating enzyme USP7 stimulates the release of pro-inflammatory mediators in acute lung injury.Journal of molecular medicine (Berlin, Germany) · 2020Article
- LncRNA NRON down-regulates lncRNA snaR and inhibits cancer cell proliferation in TNBC.Bioscience reports · 2019Article
- Repression of GCN5 expression or activity attenuates c-MYC expression in non-small cell lung cancer.American journal of cancer research · 2019Article
- Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials.Signal transduction and targeted therapyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone acetyltransferases (HATs) play vital functions in the tumorigenesis of many solid organ malignancies. We previously screened a human HATs cDNA library and identified Tat-interactive protein-60KDa (TIP60) as a candidate critical HATs in the origination of lung cancer. In this study, our data suggested that overexpression of TIP60 inhibited the cell viability of A549 and H1299 cells since day 2. Compared to the control group, the viability of these two lung cancer cells was inhibited by 25% and 19% at day 6 with the overexpression of TIP60. It increased by 36% and 26% when TIP60 was knockdown for 6 days. The invasion ability of these two cells was also restrained when TIP60 was overexpressed. While knockdown of TIP60 had the opposite effect. Inhibition of TIP60 significantly promoted the expression of molecules in AKT signaling pathway especially c-Myc. Furthermore, compared to paired tumor-adjacent tissue, lung cancer tumors had low expression of TIP60. Therefore, we concluded that TIP60 might inhibit the viability and invasion ability of lung cancer cells through down-regulation of AKT signaling pathway.
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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.