ArticlePeerJ2019
Transcriptomic study of the mechanism of anoikis resistance in head and neck squamous carcinoma.
Article in PeerJ, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 14 citations in OpenAlex.
- An anoikis-related four-gene prognostic signature and functional characterization of ANXA5 in laryngeal squamous cell carcinoma.Frontiers in immunology · 2026Article
- Development of a cancer metastasis-associated risk model via multi-machine-learning algorithms for prognostic risk evaluation and clinical application in oral squamous cell carcinoma.Journal of translational medicine · 2025Article
- Construction and validation of an anoikis-related long non-coding RNA-based prognostic model for head and neck squamous cell carcinoma.Translational cancer research · 2025Article
- Comprehensive bioinformatics analysis and experimental validation: An anoikis-related gene prognostic model for targeted drug development in head and neck squamous cell carcinoma.Oncology research · 2023Article
- Article
- Analyses of Transcriptomics Cell Signalling for Pre-Screening Applications in the Integrated Approach for Testing and Assessment of Non-Genotoxic Carcinogens.International journal of molecular sciences · 2022Review
- RNA Sequencing and Cell Models of Virus-Associated Cancer (Review).Sovremennye tekhnologii v meditsine · 2022Review
- FASN Knockdown Inhibited Anoikis Resistance of Gastric Cancer Cells via P-ERK1/2/Bcl-xL Pathway.Gastroenterology research and practice · 2021Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNormal epithelial cells rapidly undergo apoptosis as soon as they lose contact with the extracellular matrix (ECM), which is termed as anoikis. However, cancer cells tend to develop a resistance mechanism to anoikis. This acquired ability is termed as anoikis resistance. Cancer cells, with anoikis resistance, can spread to distant tissues or organs via the peripheral circulatory system and cause cancer metastasis. Thus, inhibition of anoikis resistance blocks the metastatic ability of cancer cells.
methodsAnoikis-resistant CAL27 (CAL27
resultsGO enrichment analysis indicated that the biological process (BP) of the DEGs was associated with epidermal development, DNA replication, and G1/S transition of the mitotic cell cycle. The analysis of cellular component (CC) showed that the most significant up-regulated genes were related to extracellular exosome. KEGG Pathway analysis revealed that 23 signaling pathways were activated (
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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.