ArticleEMBO reports2021
Quaking 5 suppresses TGF-β-induced EMT and cell invasion in lung adenocarcinoma.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- OTUD5-TIF1γ-SMAD3/4 positive feedback loop inhibits TGF-β-induced EMT and metastasis in NSCLC.Cell death & disease · 2026Article
- Circular RNA MALAT1 as a potential target for antimetastatic therapy.Non-coding RNA research · 2026Review
- Article
- Prognostic prediction and immune correlation analysis of anoikis- and epithelial-mesenchymal transition-related genes in lung adenocarcinoma.Translational cancer research · 2026Article
- Deciphering the Role of ADAMTS6 in the Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Cells.International journal of molecular sciences · 2025Article
- RNA-binding protein quaking: a multifunctional regulator in tumour progression.Annals of medicine · 2025Review
- Review
- Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- CCDC110 promotes the progression of hepatocellular carcinoma by activating the TGF-β/SMAD signaling pathway through targeted regulation of TGFBR1.Cancer cell international · 2025Article
- RNA-binding proteins and autophagy in lung cancer: mechanistic insights and therapeutic perspectives.Discover oncology · 2025Review
- Epithelial-mesenchymal transition in pulmonary fibrosis: molecular mechanisms and emerging therapeutic strategies.Frontiers in medicine · 2025Review
- The molecular features of lung cancer stem cells in dedifferentiation process-driven epigenetic alterations.The Journal of biological chemistry · 2024Review
- Epithelial-mesenchymal plasticity in cancer: signaling pathways and therapeutic targets.MedComm · 2024Review
- Bone-metastatic lung adenocarcinoma cells bearing CD74-ROS1 fusion interact with macrophages to promote their dissemination.Oncogene · 2024Article
- OLFM2 promotes epithelial-mesenchymal transition, migration, and invasion in colorectal cancer through the TGF-β/Smad signaling pathway.BMC cancer · 2024Article
- FOXP3-regulated lncRNA NONHSAT136151 promotes colorectal cancer progression by disrupting QKI interaction with target mRNAs.Journal of cellular and molecular medicine · 2024Article
- Upregulation of CELSR1 expression promotes ovarian cancer cell proliferation, migration, and invasion.Medical oncology (Northwood, London, England) · 2023Article
- RNA‑binding protein quaking 5 inhibits the progression of non‑small cell lung cancer by upregulating netrin‑4 expression.Oncology reports · 2023Article
- Oral squamous cell carcinomas: state of the field and emerging directions.International journal of oral science · 2023Review
- Resveratrol plays an anti-fibrotic and anti-autophagy role by stimulating miR-192-5p expression in urethral fibrosis.Functional & integrative genomics · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Quaking (QKI) proteins belong to the signal transduction and activation of RNA (STAR) family of RNA-binding proteins that have multiple functions in RNA biology. Here, we show that QKI-5 is dramatically decreased in metastatic lung adenocarcinoma (LUAD). QKI-5 overexpression inhibits TGF-β-induced epithelial-mesenchymal transition (EMT) and invasion, whereas QKI-5 knockdown has the opposite effect. QKI-5 overexpression and silencing suppresses and promotes TGF-β-stimulated metastasis in vivo, respectively. QKI-5 inhibits TGF-β-induced EMT and invasion in a TGFβR1-dependent manner. KLF6 knockdown increases TGFβR1 expression and promotes TGF-β-induced EMT, which is partly abrogated by QKI-5 overexpression. Mechanistically, QKI-5 directly interacts with the TGFβR1 3' UTR and causes post-transcriptional degradation of TGFβR1 mRNA, thereby inhibiting TGF-β-induced SMAD3 phosphorylation and TGF-β/SMAD signaling. QKI-5 is positively regulated by KLF6 at the transcriptional level. In LUAD tissues, KLF6 is lowly expressed and positively correlated with QKI-5 expression, while TGFβR1 expression is up-regulated and inversely correlated with QKI-5 expression. We reveal a novel mechanism by which KLF6 transcriptionally regulates QKI-5 and suggest that targeting the KLF6/QKI-5/TGFβR1 axis is a promising targeting strategy for metastatic LUAD.
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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.