ArticleBreast cancer research : BCR2010
Silencing of the IKKε gene by siRNA inhibits invasiveness and growth of breast cancer cells.
Article in Breast cancer research : BCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 62 citations in OpenAlex.
- Small interfering RNA (siRNA)-based targeting breast cancer therapy.Discover oncology · 2026Review
- Cholesterol modified defense peptide as an EMP2-siRNA delivery system for synergistic immunogene therapy against breast cancer.Materials today. Bio · 2025Article
- Therapeutic delivery of siRNA for the management of breast cancer and triple-negative breast cancer.Therapeutic delivery · 2024Review
- Suppression of E6 Oncogene Induces Apoptosis in CaSki Cervical Cancer Cells.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- siRNA and targeted delivery systems in breast cancer therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Development of amino acid-modified biodegradable lipid nanoparticles for siRNA delivery.Acta biomaterialia · 2022Article
- Article
- Sanguinarine Inhibition of TNF-α-Induced CCL2, IKBKE/NF-κB/ERK1/2 Signaling Pathway, and Cell Migration in Human Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Nanotechnological Approaches for the Treatment of Triple-Negative Breast Cancer: A Comprehensive Review.Current drug metabolism · 2022Review
- IκB kinase-ε-mediated phosphorylation triggers IRF-1 degradation in breast cancer cells.Neoplasia (New York, N.Y.) · 2020Article
- Bioengineered siRNA-Based Nanoplatforms Targeting Molecular Signaling Pathways for the Treatment of Triple Negative Breast Cancer: Preclinical and Clinical Advancements.Pharmaceutics · 2020Review
- Molecular mechanism of gossypol mediating CCL2 and IL‑8 attenuation in triple‑negative breast cancer cells.Molecular medicine reports · 2020Article
- The Specific IKKε/TBK1 Inhibitor Amlexanox Suppresses Human Melanoma by the Inhibition of Autophagy, NF-κB and MAP Kinase Pathways.International journal of molecular sciences · 2020Article
- Co-delivery of IKBKE siRNA and cabazitaxel by hybrid nanocomplex inhibits invasiveness and growth of triple-negative breast cancer.Science advances · 2020Article
- Advances in IKBKE as a potential target for cancer therapy.Cancer medicine · 2020Review
- Oncogenic Signaling in Tumorigenesis and Applications of siRNA Nanotherapeutics in Breast Cancer.Cancers · 2019Review
- Expression and prognostic role of IKBKE and TBK1 in stage I non-small cell lung cancer.Cancer management and research · 2019Article
- IΚΚε cooperates with either MEK or non-canonical NF-kB driving growth of triple-negative breast cancer cells in different contexts.BMC cancer · 2018Article
- Development of a peptide-modified siRNA nanocomplex for hepatic stellate cells.Nanomedicine : nanotechnology, biology, and medicine · 2018Article
- A database of breast oncogenic specific siRNAs.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
introductionIκB Kinase ε (IKKε) is a member of the IKK family which plays an important role in the activation of nuclear factor-κB (NF-κB). Overexpressed in over 30% of breast cancers, IKKε has been recently identified as a potential breast cancer oncogene. The purpose of this study is to examine the therapeutic potential of IKKε siRNA on human breast cancer cells.
methodsEight siRNAs targeting different regions of the IKKε mRNA were designed, and the silencing effect was screened by quantitative real time RT-PCR. The biological effects of synthetic siRNAs on human breast cancer cells were investigated by examining the cell proliferation, migration, invasion, focus formation, anchorage-independent growth(via soft agar assay), cell cycle arrest, apoptosis (via annexing binding), NF-κB basal level, and NF-κB related gene expressions upon the IKKε silencing.
resultsSilencing of IKKε in human breast cancer cells resulted in decrease of focus formation potential and clonogenicity as well as in vitro cell migration/invasion capabilities. Moreover, knockdown of IKKε suppressed cell proliferation. Cell cycle assay showed that the anti-proliferation effect of IKKε siRNA was mediated by arresting cells in G(0)/G(1) phase, which was caused by down-regulation of cyclin D(1). Furthermore, we demonstrated that silencing of IKKε inhibited the NF-κB basal activity as well as the Bcl-2 expression. Significant apoptosis was not observed in breast cancer cells upon the silencing of IKKε. The present study provided the first evidence that silencing IKKε using synthetic siRNA could inhibit the invasiveness properties and proliferation of breast cancer cells.
conclusionsOur results suggested that silencing IKKε using synthetic siRNA may offer a novel therapeutic strategy for breast cancer.
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.