ArticleOncoTargets and therapy2019
Circular RNA hsa_circ_0023404 promotes proliferation, migration and invasion in non-small cell lung cancer by regulating miR-217/ZEB1 axis.
Article in OncoTargets and therapy, 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 It has been retracted, and should not be counted.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 22 papers.
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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
22 citing papers in PubMed, 41 citations in OpenAlex.
- Deciphering the impact of circRNA-mediated autophagy on tumor therapeutic resistance: a novel perspective.Cellular & molecular biology letters · 2024Review
- Exosomal circular RNA: a signature for lung cancer progression.Cancer cell international · 2022Review
- Circular RNA hsa_circ_0023404 promotes the proliferation, migration and invasion in endometrial cancer cells through regulating miR-217/MAPK1 axis.European journal of medical research · 2022Article
- The FUS/circEZH2/KLF5/ feedback loop contributes to CXCR4-induced liver metastasis of breast cancer by enhancing epithelial-mesenchymal transition.Molecular cancer · 2022Article
- Circular RNA circ_0023404 serves as a miR-636 sponge to promote malignant behaviors in cervical cancer cells through upregulation of CYP2S1.The Kaohsiung journal of medical sciences · 2022Article
- The circROBO1/KLF5/FUS feedback loop regulates the liver metastasis of breast cancer by inhibiting the selective autophagy of afadin.Molecular cancer · 2022Article
- Calycosin Inhibits the Malignant Behaviors of Lung Adenocarcinoma Cells by Regulating the circ_0001946/miR-21/GPD1L/HIF-1Disease markers · 2022Article
- CircZNF124 regulates cell proliferation, leucine uptake, migration and invasion by miR-199b-5p/SLC7A5 pathway in endometrial cancer.Immunity, inflammation and disease · 2021Article
- Circular RNAs regulate cancer-related signaling pathways and serve as potential diagnostic biomarkers for human cancers.Cancer cell international · 2021Review
- Circ_0023404 sponges miR-136 to induce HK-2 cells injury triggered by hypoxia/reoxygenation via up-regulating IL-6R.Journal of cellular and molecular medicine · 2021Article
- hsa_circ_0058357 acts as a ceRNA to promote non‑small cell lung cancer progression via the hsa‑miR‑24‑3p/AVL9 axis.Molecular medicine reports · 2021Article
- MicroRNA-217 inhibits the proliferation and invasion, and promotes apoptosis of non-small cell lung cancer cells by targeting sirtuin 1.Oncology letters · 2021Article
- Circular RNAs in Lung Cancer: Recent Advances and Future Perspectives.Frontiers in oncology · 2021Review
- Insights Into circRNAs: Functional Roles in Lung Cancer Management and the Potential Mechanisms.Frontiers in cell and developmental biology · 2021Review
- Circular RNA circ-LDLRAD3 serves as an oncogene to promote non-small cell lung cancer progression by upregulating SLC1A5 through sponging miR-137.RNA biology · 2020Article
- MicroRNAs and Their Influence on the ZEB Family: Mechanistic Aspects and Therapeutic Applications in Cancer Therapy.Biomolecules · 2020Review
- Circular RNA circ_0001105 Inhibits Progression and Metastasis of Osteosarcoma by Sponging miR-766 and Activating YTHDF2 Expression.OncoTargets and therapy · 2020Article
- Circ_100565 promotes proliferation, migration and invasion in non-small cell lung cancer through upregulating HMGA2 via sponging miR-506-3p.Cancer cell international · 2020Article
- CircDENND2A Promotes Non-small Cell Lung Cancer Progression via Regulating MiR-34a/CCNE1 Signaling.Frontiers in genetics · 2020Article
- Circ_0007142/miR-186/FOXK1 axis promoted lung adenocarcinoma progression.American journal of translational research · 2020Article
Corrections and comments
- Retraction · 2024-04-03Author Unresponsive · Concerns/Issues about Image · Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCircular RNAs (circRNAs) have been considered as key regulators of cancer biology. However, the functional role of hsa_circ_0023404 in non-small cell lung cancer (NSCLC) and its regulatory mechanism are still almost unknown.
methodsThe expression of hsa_circ_0023404, miR-217 and zinc finger E-box-binding homeobox 1 (ZEB1) was evaluated by quantitative real-time polymerase chain reaction. The role of hsa_circ_0023404 in NSCLC progression was determined using cell count kit-8 assay, transwell migration and invasion assay. Luciferase reporter assay was performed to assess the interaction of hsa_circ_0023404, miR-217 and ZEB1 in NSCLC cells.
resultsThe expression of hsa_circ_0023404 was upregulated in NSCLC tissues, as well as in NSCLC cell lines. High hsa_circ_0023404 expression predicted short overall survival in NSCLC. Functionally, knockdown of hsa_circ_0023404 inhibited the proliferation, migration and invasion of NSCLC cells. In the further molecular mechanism study, hsa_circ_0023404 was shown to interact with miR-217/ZEB1 axis to contribute to the growth of NSCLC cells.
conclusionhsa_circ_0023404 promotes the proliferation, migration and invasion of NSCLC cells by regulating miR-217/ZEB1 axis, providing a fresh perspective on circRNAs in NSCLC development.
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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.