ArticleCancer biotherapy & radiopharmaceuticals2015
Lentivirus-Mediated Knockdown of Myosin VI Inhibits Cell Proliferation of Breast Cancer Cell.
Article in Cancer biotherapy & radiopharmaceuticals, 2015. 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 It has been retracted, and should not be counted. It is linked to trial NCT03430024 (Nuclear Myosin VI - a Therapeutic Target in Estrogen Receptor Positive Breast Cancer?), which is not on this map. Cited by 13 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.
Nuclear Myosin VI - a Therapeutic Target in Estrogen Receptor Positive Breast Cancer?
Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- MYO6 contributes to tumor progression and enzalutamide resistance in castration-resistant prostate cancer by activating the focal adhesion signaling pathway.Cell communication and signaling : CCS · 2024Article
- A planar polarized MYO6-DOCK7-RAC1 axis promotes tissue fluidification in mammary epithelia.Cell reports · 2023Article
- Binding partners regulate unfolding of myosin VI to activate the molecular motor.The Biochemical journal · 2022Article
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- Article
- Review
- Long noncoding RNA UCA1 promotes cell growth, migration, and invasion by targeting miR-143-3p in oral squamous cell carcinoma.Cancer medicine · 2020Article
- The Expressions and Mechanisms of Sarcomeric Proteins in Cancers.Disease markers · 2020Review
- HNF1A-AS1 Regulates Cell Migration, Invasion and Glycolysis via Modulating miR-124/MYO6 in Colorectal Cancer Cells.OncoTargets and therapy · 2020Article
- BAG3 Overexpression and Cytoprotective Autophagy Mediate Apoptosis Resistance in Chemoresistant Breast Cancer Cells.Neoplasia (New York, N.Y.) · 2018Article
- Profiling plasma extracellular vesicle by pluronic block-copolymer based enrichment method unveils features associated with breast cancer aggression, metastasis and invasion.Journal of extracellular vesicles · 2018Article
- NDP52 activates nuclear myosin VI to enhance RNA polymerase II transcription.Nature communications · 2017Article
- miR-143 and miR-145 inhibit gastric cancer cell migration and metastasis by suppressing MYO6.Cell death & disease · 2017Article
Corrections and comments
- Retraction · 2021-09-30Duplication of Data · Duplication of Text · Investigation by Journal/Publisher · Paper Mill ·
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myosin VI (MYO6) is a unique member of the myosin superfamily, and almost no experimental studies link MYO6 to tumorigenesis of breast cancer. However, previous microarray data demonstrated that MYO6 was frequently overexpressed in breast cancer tissues. In this study, to further develop its role in breast cancer, endogenous expression of MYO6 was significantly inhibited in breast cancer ZR-75-30 and MDA-MB-231 cells using lentivirus-mediated RNA interference. Quantitative polymerase chain reaction and western blot were applied to detect the expression level of MYO6. Cell viability of both cell lines was measured by methylthiazol tetrazolium and colony formation assays. Besides, cell cycle assay was utilized to acquire the distribution information of cell phase. The results demonstrated that knockdown of MYO6 markedly reduced cell viability and colony formation, as well as suppressed cell cycle progression in breast cancer cells. The results suggested that MYO6 played a vital role in breast cancer cells and might provide useful information for diagnosis and therapy of human breast cancer in future.
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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.