ArticleCell death & disease2020
SKIL facilitates tumorigenesis and immune escape of NSCLC via upregulating TAZ/autophagy axis.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 45 citations in OpenAlex.
- cGAS-STING pathway in lung cancer and emerging therapeutic approaches.Drug discovery today · 2026Review
- CDNFE suggests FNDC3B and NECTIN4 as drivers of precancer progression via PI3K/AKT EMT.NPJ precision oncology · 2026Article
- Mechanotransduction-Induced Gene Expression Reveals Activation of TGFβ/SKIL/TAZ Axis and Supports Invasive Phenotype in Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Targeting super-enhancer-driven SKIL transcription by CDK7 inhibitor THZ1 to suppress gastric cancer progression.Journal of translational medicine · 2026Article
- Personalized Cancer Immunotherapy Boosted by cGAS-STING-Targeted Nanovaccines in Combination With Nutrient Modulation.Exploration (Beijing, China) · 2025Article
- Beckwith-Wiedemann syndrome and large offspring syndrome involve alterations in methylome, transcriptome, and chromatin configuration.NAR molecular medicine · 2025Article
- Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025Review
- Exploring ferroptosis and miRNAs: implications for cancer modulation and therapy.Molecular and cellular biochemistry · 2025Review
- Autophagy in tumor immune escape and immunotherapy.Molecular cancer · 2025Review
- Hypoxia-induced autophagy in pancreatic cancer counteracts the cytotoxicity of CD8Genes and immunity · 2025Article
- Combination adjuvant improves influenza virus immunity by downregulation of immune homeostasis genes in lymphocytes.ImmunoHorizons · 2025Article
- A seven-LncRNA signature for prognosis prediction of patients with lung squamous cell carcinoma through tumor immune escape.Frontiers in oncology · 2025Article
- CD248 induces PD-L1 expression on cancer-associated fibroblasts to promote NSCLC immune escape.Frontiers in cell and developmental biology · 2025Article
- Lung cancer tumor immune microenvironment: analyzing immune escape mechanisms and exploring emerging therapeutic targets.Frontiers in immunology · 2025Review
- Mast cell - tumor cell interaction related gene and microRNA expression profiles in oral squamous cell carcinoma.Frontiers in oncology · 2025Article
- Comparative Copy Number Variation Profiling of GL01, an Immortalized Non-small Cell Lung Cancer Cell Line Derived from a Filipino Patient, and A549 Lung Adenocarcinoma Cells.Acta medica Philippina · 2025Article
- Combining single-cell and bulk RNA sequencing, NK cell marker genes reveal a prognostic and immune status in pancreatic ductal adenocarcinoma.Scientific reports · 2024Article
- Role of STING in the treatment of non-small cell lung cancer.Cell communication and signaling : CCS · 2024Review
- NSUN2 promotes colorectal cancer progression by enhancing SKIL mRNA stabilization.Clinical and translational medicine · 2024Article
- Role of YAP Signaling in Regulation of Programmed Cell Death and Drug Resistance in Cancer.International journal of biological sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune escape is an important mechanism in tumorigenesis. The aim of this study was to investigate roles of SKIL in tumorigenesis and immune escape of non-small-cell lung cancer (NSCLC). SKIL expression levels in NSCLC cell line, clinical sample, and adjacent normal tissue were measured by quantitative PCR, western blot, or immunohistochemistry. Lentivirus was used to overexpress/silence SKIL or TAZ expression. Malignant phenotypes of NSCLC cells were evaluated by colony formation, transwell, and MTT assays, and in xenograft mice model. Syngeneic mice model and flow cytometry were used to evaluate T cell infiltration. Quantitative PCR and western blot were applied to evaluate relevant mRNA and protein levels, respectively. Co-immunoprecipitation was applied to unveil the interaction between SKIL and TAZ. SKIL expression was higher in NSCLC tissue compared to adjacent normal tissue. Silencing of SKIL inhibited malignant phenotypes of NSCLC cells and promoted T cell infiltration. SKIL-knockdown inhibited autophagy and activated the STING pathway in NSCLC cells through down-regulation of TAZ. Silencing of TAZ cancelled the effects of SKIL overexpression on malignant phenotypes and autophagy of NSCLC cells. Inhibition of autophagy reversed the effects of SKIL/TAZ overexpression on the STING pathway. In conclusion, SKIL promoted tumorigenesis and immune escape of NSCLC cells through upregulation of TAZ/autophagy axis and inhibition on downstream STING pathway.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.