ArticleOncogene2014
Role of tumor necrosis factor alpha-induced protein 1 in paclitaxel resistance.
Article in Oncogene, 2014. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- The emerging role of the KCTD proteins in cancer.Cell communication and signaling : CCS · 2021Review
- Circ0001320 inhibits lung cancer cell growth and invasion by regulating TNFAIP1 and TPM1 expression through sponging miR-558.Human cell · 2021Article
- Cullin3-TNFAIP1 E3 Ligase Controls Inflammatory Response in Hepatocellular Carcinoma Cells via Ubiquitination of RhoB.Frontiers in cell and developmental biology · 2021Article
- The CRL3Signal transduction and targeted therapy · 2020Article
- Tumor Necrosis Factor Alpha-Induced Proteins in Malignant Tumors: Progress and Prospects.OncoTargets and therapy · 2020Review
- Superhero Rictor promotes cellular differentiation of mouse embryonic stem cells.Cell death and differentiation · 2019Article
- Proinflammatory Factors Mediate Paclitaxel-Induced Impairment of Learning and Memory.Mediators of inflammation · 2018Article
- Article
- CXCL12 overexpression promotes the angiogenesis potential of periodontal ligament stem cells.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paclitaxel has been extensively used as an antitumor drug to treat a broad range of epithelial cancers, including breast and cervical cancers. However, the efficacy of this drug is greatly limited by the development of acquired resistance. Identification of the underlying resistance mechanisms may inform the development of new therapies that elicit long-term response of tumors to paclitaxel treatment. Here we report that increased expression of TNFAIP1 (tumor necrosis factor alpha-induced protein 1) confers acquired resistance to paclitaxel. TNFAIP1 is shown to compete with paclitaxel for binding to β-tubulin, thereby preventing paclitaxel-induced tubulin polymerization, cell cycle arrest and ultimate cell death. We also show that expression of TNFAIP1 is regulated by the transcriptional factor Sp1. In a xenograft mouse model, increased expression of TNFAIP1 decreases, whereas knockdown of TNFAIP1 increases tumor response to paclitaxel. Therefore, these results reveal tnfaip1 as a novel paclitaxel-resistance associated gene and suggest that TNFAIP1 may represent a valuable therapeutic target for the treatment of cancer.
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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.