ArticleCell proliferation2019
Six2 promotes non-small cell lung cancer cell stemness via transcriptionally and epigenetically regulating E-cadherin.
Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Natural product mediated mesenchymal-epithelial remodeling by covalently binding ENO1 to degrade m6A modifiedActa pharmaceutica Sinica. B · 2025Article
- The SIX2/PFN2 feedback loop promotes the stemness of gastric cancer cells.Journal of translational medicine · 2024Article
- Integrated analysis reveals a novel 5-fluorouracil resistance-based prognostic signature with promising implications for predicting the efficacy of chemotherapy and immunotherapy in patients with colorectal cancer.Apoptosis : an international journal on programmed cell death · 2024Article
- Chemoresistance Mechanisms in Non-Small Cell Lung Cancer-Opportunities for Drug Repurposing.Applied biochemistry and biotechnology · 2024Review
- SIX2 promotes cell plasticity via Wnt/β-catenin signalling in androgen receptor independent prostate cancer.Nucleic acids research · 2024Article
- Transcription factor-target gene regulatory network analysis in human lung adenocarcinoma.Journal of thoracic disease · 2023Article
- SIX3 function in cancer: progression and comprehensive analysis.Cancer gene therapy · 2022Review
- Review
- Transcription of the Envelope Protein by 1-L Protein-RNA Recognition Code Leads to Genes/Proteins That Are Relevant to the SARS-CoV-2 Life Cycle and Pathogenesis.Current issues in molecular biology · 2022Article
- High-Intensity Aerobic Exercise Suppresses Cancer Growth by Regulating Skeletal Muscle-Derived Oncogenes and Tumor Suppressors.Frontiers in molecular biosciences · 2022Article
- Corrigendum.Cell proliferation · 2021Article
- The SIX Family of Transcription Factors: Common Themes Integrating Developmental and Cancer Biology.Frontiers in cell and developmental biology · 2021Review
- Development and Validation of a Robust Pyroptosis-Related Signature for Predicting Prognosis and Immune Status in Patients with Colon Cancer.Journal of oncology · 2021Article
- Silencing of CASC8 inhibits non-small cell lung cancer cells function and promotes sensitivity to osimertinib via FOXM1.Journal of Cancer · 2021Article
- Kinesin family member 2A promotes cancer cell viability, mobility, stemness, and chemoresistance to cisplatin by activating the PI3K/AKT/VEGF signaling pathway in non-small cell lung cancer.American journal of translational research · 2021Article
- Dysregulation of cancer genes by recurrent intergenic fusions.Genome biology · 2020Article
- Article
- Six2 promotes non-small cell lung cancer cell stemness via transcriptionally and epigenetically regulating E-cadherin.Cell proliferation · 2019Article
Corrections and comments
- Correction · 2021-06-01Error in Image · Updated to Retraction ·
- Retraction · 2024-05-28Euphemisms for Plagiarism · Investigation by Journal/Publisher · Original Data and/or Images not Provided and/or not Available · Plagiarism of Image · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) ·
- Erratum issuedCorrigendum.2021
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectivesThe roles and related mechanisms of six2 in regulating non-small cell lung cancer (NSCLC) cells progression are unclear. This work aimed to explore the roles of six2 in NSCLC cell stemness. MATERIALS AND
methodsKaplan-Meier plotter analysis was used to examine the correlation between six2 expression and the survival of NSCLC patients. Quantitative reverse transcription PCR and Western blot were performed to detect six2 expression in clinical samples. Moreover, transwell migration, tumour spheroid formation and in vivo tumour formation assays were used to examine the effects of six2 on NSCLC cell progression. Additionally, methylation analysis was carried out to measure E-cadherin methylation level in different cells. Finally, cell viability assay was performed to explore the effects of six2 on chemotherapeutic sensitivity of NSCLC cells.
resultsLung cancer patients with a higher six2 expression level displayed a shorter overall survival. Six2 expression was higher in lung cancer tissues than in normal adjacent tissues. Additionally, six2 knockdown suppressed NSCLC cell stemness. Mechanistically, six2 overexpression inhibited epithelial marker E-cadherin expression via stimulating its promoter methylation. And E-cadherin knockdown rescued six2 knockdown-induced decrease of NSCLC cancer cell stemness. Notably, six2 knockdown enhanced cisplatin sensitivity in parental NSCLC cells and attenuated cisplatin resistance in cisplatin-resistant NSCLC cells.
conclusionsOur results suggest that six2 facilitates NSCLC cell stemness and attenuates chemotherapeutic sensitivity via suppressing E-cadherin expression.
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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.