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My accountHeLa cells stably silenced: SilenciX KD cell lines
See the related productsSilenciX®: HeLa cells stably silenced for your gene of interest
The SilenciX® technology has been proven to be a robust cellular model (from HeLa cells or other cell lines) that brings valuable insights into cellular pathways when performing cell signalling studies, proof of concept (PoC) studies or indentifying mechanisms of action (MoA)) as well as drug screening, within a cellular environment of a stably silenced gene target (see Nature Methods 5 March 2008).
What is SilenciX®?
SilenciX® cells are tebu-bio's ready-to-use, knockdown (KD) cell lines using a unique siRNA Delivery system.
The most classic approaches to silencing are based on siRNA but these strategies suffer from lack of stability and efficiency.
To overcome this issue, new tools based on short hairpin (shRNA) have been developed. These tools increase stability, but disturb genome integrity.
Our solution
The SilenciX® technology combines RNAi technology, EBV derived vectors and a Designer of Small Interfering RNA (DSIR) program.
This enables the generation of syngenic, ready-to-use and stable cellular in vitro models stably silenced for a gene of interet.
This technology has already been validated in the scientific literature in various biological domains and applications such as DNA Repair, Epigenetics, Ubiquitination and the cell cycle, Drug discovery, cell signalling and mechanism of action.
SilenciX® benefits & advantages
The SilenciX® technology brings stability and efficiency of knockdown in a syngenic model at an affordable cost.
More than one hundred ready-to-use models with specific and efficient knockdown are already available.
- High silencing efficiency
We obtain >80% KD (tebu-bio quality controls are performed by qPCR) leading to very low remaining gene expression in SilenciX®, compared to endogenous expression.
- KD stability - more than 500 days in culture
Stable silencing over time (months) reinforced with hygromycine selection
- Syngenic Cell Lines
No integration into the genome - vector remains anchored to the chromosomes giving access to comparable genetic background between cell line control and knock-down.
- Safe, virus-free and in vitro liposomal transfection
Long-term gene silencing without the safety concerns inherent in viral-based siRNA vehicles.
From HeLa cell line to fully customized cell lines, there's a SilenciX® suited to your needs...
The SilenciX technology is available as catalogue products (HeLa cells stably silenced for a gene of interest). Nevertheless, our laboratories can design and develop for you custom SilenciX cell lines from your cell lines.
personalised solutions for your project.
Complete: what you'll receive in your SilenciX® HeLa cell line kit...
- 1 vial of target specific SilenciX® cells
- 1 vial of control SilenciX® cells (transfected with a non-relevant shRNA sequence)
- Specification sheets with quantatitive PCR quality controls
- Complete User Manual
Ready-to-use: getting started with your SilenciX®.HeLa cells..
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Flexible: Custom SilenciX® on simple request
Can't see your SilenciX® in our catalogue? Just let us know your cell type of interest and your target gene and we'll send you a personalised quotation. Our product specialists will be more than pleased to suggest the ideal solutions for your project.
SilenciX® technology has already been shown to be compatible with numerous mammalian cell types including Human, Primate and Rodent cells.
For further information or for any queries, get in touch with your local tebu-bio office.
Proven, guaranteed technology:
Main SilenciX® applications
Since they were established, SilenciX® cell lines have been used in a wide variety of fields. They are especially appreciated in genetic disease and cancer studies, where the difficulty is to study protein loss-of-function in a stable genetic background.
A large number of applications directly linked to drug development can be seen in the literature :
Loss-of-function & cell signalling model
Silencing is today the most adopted method to study gene function.
SilenciX® combines RNAi technology, a DSIR Program and a pEBV (Epstein Barr Virus) derived vector to generate functional stable knock-down clones to study protein loss-of-function.
Click here to download our SilenciX® application poster
- How SilenciX® cell lines have proven their use as Loss of Function models & mechanistic insights...
Nucleocytoplasmic Translocation of UBXN2A Is Required for Apoptosis during DNA Damage Stresses in Colon Cancer Cells.
Abdullah A. et al. (Sept 2015) J. Cancer 2015, 6, 11, 1066–1078. DOI: 10.7150/jca.12134.
UCP2 modulates single-channel properties of a MCU-dependent Ca2+ inward current in mitochondria.
Bondarenko A.I. et al. (2015) Eur. J. Physiol. 467:2509–2518. DOI 10.1007/s00424-015-1727-z.
Poly(ADP-Ribosyl) Glycohydrolase Prevents the Accumulation of Unusual Replication Structures during Unperturbed S Phase.
Chaudhuri A.R. et al. (2015) Mol. Cell. Biol., vol 35, 5, 856-865. DOI: 10.1128/MCB.01077-14.
A DNA-dependent stress response involving DNA-PK occurs in hypoxic cells and contributes to cellular adaptation to hypoxia
Bouquet F, et al., J Cell Sci. 2011 Jun 1;124(Pt 11):1943-51
Activation of NRF2 by nitrosative agents and H2O2 involves KEAP1 disulfide formation
Fourquet S. et al., J Biol Chem. 2010 Mar 12;285(11):8463-71
ARTEMIS nuclease facilitates apoptotic chromatin cleavage
Britton S. et al., Cancer Res. 2009 Oct 15;69(20):8120-6
Differential contribution of XPC, RAD23A, RAD23B and CENTRIN 2 to the UV-response in Human cells
Renaud E, et al., DNA Repair 2011 Aug 15;10(8):835-47
Interplay between Cernunnos-XLF and nonhomologous end-joining proteins at DNA ends in the cell
Wu et al., J Biol Chem. 2007 Nov 2;282(44):31937-43
Long-term XPC silencing reduces DNA double-strand break repair
Despras et al., Cancer Res. 2007; 67: 2526-2534.
Loss of ATM positively regulates the expression of Hypoxia Inducible Factor 1 (HIF-1) through oxidative stress: role in the physiopathology of the disease
Ousset M, et al., Cell Cycle 2010 Jul 3;9 (14)
NER factors are recruited to active promoters and facilitate chromatin modification for transcription in the absence of exogenous genotoxic attack
Le May N. et al., Mol Cell. 2010 Apr 9;38(1):54-66
Partial complementation of a DNA ligase I deficiency by DNA ligase III and its impact on cell survival and telomere stability in mammalian cells
Le Chalony, et al., Cell Mol Life Sci. 2012
Poly (ADP-Ribose) Glycohydrolase Regulates Retinoic Acid Receptor-Mediated Gene Expression
Le May N, Mol Cell. 2012 Oct 24. pii: S1097-2765(12)00821-0. doi:
10.1016/j.molcel.2012.09.021
Role of ATM in the telomere response to the G-quadruplex ligand 360A
Pennarun G. et al., Nucleic Acids Res. 2008 Mar;36(5):1741-54
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Synthetic Lethality
Synthetic lethality occurs when 2 separate genes compensate for each other in term of function:
- If only one gene is mutated, then the other compensates and function is maintained
- If both genes are mutated, then function is lost and phenotype appears (here death)
One of the challenges in this approach is to validate synthetic lethal genes.
Our solution has been to design SilenciX® cell lines in which a gene known to be implicated in synthetic lethality is already silenced.
By comparing the control and the silenced cell lines, the target can be easily explored.
Examples of SilenciX® for Synthetic Lethality studies
| Target Name | Level of KD | Cat. Nr. |
|---|---|---|
| BRCA1 | 86% | 01-00041 |
| BRCA2 | 72% | 01-00028 |
| XRCC1 | 87% | 01-00017 |
| PARP1 | 97% | 01-00019 |
| PARP2 | 86% | 01-00020 |
| APE1 | >70% | 01-00155 |
tebu-bio quality controls are performed by qPCR
- How SilenciX® cell lines have proven their use in Synthetic Lethality research...
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New publication using the SilenciX cellular models:
Cellularly active N-hydroxyurea FEN1 inhibitors block substrate entry to the active site.
Exell J.C. et al. (August 2016) Nature Chemical Biology 12, 815–821 (2016) doi:10.1038/nchembio.2148.
A BRCA2 specific knoch-down stable cellular model to screen molecular targets with the Synthetic Lethality approach. Anne Marie Renault (tebu-bio), Helen Robinson (MISSION Therapeutics), et al. (poster at the Cancer Pharmacogenomics and Targeted Therapies congress). September 2013
Inhibition of DNA damage repair by artificial activation of PARP with siDNA.
Croset A, et al. Nucleic Acids Res. 2013 August.
Synthetic lethal targeting of DNA double-strand break repair deficient cells by human apurinic/apyrimidinic endonuclease inhibitors.
Sultana, et al. Int J Cancer. 2012 Nov 15;131(10):2433-44. doi:10.1002/ijc.27512. Epub 2012 Mar 28.
Targeting XRCC1 deficiency in breast cancer for personalized therapy.
Sultana R, et al. Cancer Res. 2012 Dec 19.
Personalized medicine
New tools in molecular biology have given rise to of a new area of research: personalized medicine.
It is a customization of healthcare with decision and practices being tailored to the individual patient by use of genetic or other information (Biomarkers). Combining this information gives an indication of whether there is a threat for disease, whether a disease already exists, or how such disease may develop in an individual case.
The discovery of polymorphism in genes that function in the metabolism of chemicals and in DNA repair has demonstrated the importance of understanding the phenomenon of genetic susceptibility in a population.
Another incoming important challenge in personalized medicine and in drug discovery is the prediction of the population on which a drug can be used. The sooner this evaluation is done in development, the more adapted the process can be.
A new application of SilenciX® is to allow researchers to test their components on a cell line which mimics the population of interest.
Examples of SilenciX® for Personalised Medicine studies
| Target Name | Level of KD | Cat. Nr. |
|---|---|---|
| BRCA1 | 86% | 01-00041 |
| BRCA2 | 72% | 01-00028 |
| XRCC1 | 87% | 01-00017 |
| OGG1 | 97% | 01-00014 |
| NEIL2 | 81% | 01-00053 |
| MSH2 | 91% | 01-00023 |
| MLH1 | >70% | 01-00147 |
tebu-bio quality controls are performed by qPCR
- How SilenciX® cell lines have proven their use in Personalised Medicine research...
Targeting BRCA1-BER deficient breast cancer by ATM or DNA-PKcs blockade either alone or in combination with cisplatin for personalized therapy.
Albarakatia N. et al. (2015) Molecular Oncology 9, 1, 204–217. DOI:10.1016/j.molonc.2014.08.001.
Long-term XPC silencing reduces DNA double-strand break repair.
Despras et al., Cancer Res. 2007; 67: 2526-2534.
Oxidation-mediated DNA cross-linking contributes to the toxicity of 6-thioguanine in human cells.
Brem, et al. Cancer Res. 2012 Sep
Synthetic lethal targeting of DNA double-strand break repair deficient cells by human purinic/apyrimidinic endonuclease inhibitors.
Sultana, et al. Int J Cancer. 2012 Nov 15;131(10):2433-44. doi:10.1002/ijc.27512. Epub 2012 Mar 28.
The impact of cyclin-dependent kinase 5 depletion on poly(ADPribose) polymerase activity and responses to radiation.
Bolin C, et al., Cell Mol Life Sci. 2011 Sept 16.
Clinicopathological and functional significance of XRCC1 expression in ovarian cancer.
Abdel-Fatah T, et al. Int J Cancer. 2012 Dec 6. doi: 10.1002/ijc.27980.
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Drug Selectivity
To allow researchers to verify the efficiency of inhibitors, we have developed a family of cell lines for new attractive targets in research.
Examples of SilenciX® for Drug Selectivity studies
| Target Name | Level of KD | Cat. Nr. |
|---|---|---|
| USP7 | 74% | 01-00159 |
| USP9X | 73% | 01-00160 |
| DNA-PKcs | 93% | 01-00005 |
| APE1 | >70% | 01-00155 |
| PARP1 | 97% | 01-00019 |
| PARP2 | 86% | 01-00020 |
tebu-bio quality controls are performed by qPCR
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Human disease mimicking model
Comparison of cells derived from patients with the same phenotype or disease can be problematic due to their different genetic backgrounds.
SilenciX® cell lines mimic the behavior of cells derived from patients and enable you to assess the long-term consequences of gene silencing in a robust model.
Click here to download our SilenciX® application poster
Examples of SilenciX® for Human Disease Mimicking Models
| Target Name | Level of KD | Cat. Nr. |
|---|---|---|
| XPA | 78% | 01-00015 |
| XPC | 81% | 01-00016 |
| ATR | 70% | 01-00025 |
| ATM | 88% | 01-00029 |
| BRCA1 | 86% | 01-00041 |
| BRCA2 | 72% | 01-00028 |
| FANCD1 | 85% | 01-00027 |
tebu-bio quality controls are performed by qPCR
- How SilenciX® cell lines have proven their use for Human Disease Mimicking Models...
ATR contributes to telomere maintenance in human cells
Pennarun G. et al., Nucleic Acids Res. 2010 May;38(9):2955-63
Long-term XPC silencing reduces DNA double-strand break repair.
Despras et al., Cancer Res. 2007; 67: 2526-2534.
Loss of ATM positively regulates the expression of Hypoxia Inducible Factor 1 (HIF-1) through oxidative stress: role in the physiopathology of the disease
Ousset M, et al., Cell Cycle 2010 Jul 3;9 (14)
NER factors are recruited to active promoters and facilitate chromatin modification for transcription in the absence of exogenous genotoxic attack
Le May N. et al., Mol Cell. 2010 Apr 9;38(1):54-66
NF-κB regulates DNA double-strand break repair in conjunction with BRCA1–CtIP complexes
Volcic, et al. Nucleic Acids Res. (2012)
Untangling the relationships between DNA repair pathways by silencing more than 20 DNA repair genes in human stable clones.
Biard, Nucleic Acids Res. 2007;35(11):3535-50
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SilenciX® has been used to find genes that, when silenced, result in sensitivity to certain chemotherapy treatments. Researchers therefore can further characterize drug-sensitive targets and novel drug combinations that sensitize cancer cells to chemotherapeutic drugs.
More than 100 cell lines are already available from catalogue, or get in touch with our specialists for your custom requests.
- How SilenciX® cell lines have proven their use for Therapy Combination...
PRX1 knockdown potentiates vitamin K3 toxicity in cancer cells: a potential new therapeutic perspective for an old drug.
Tiantian, H. at al. Journal of Experimental & Clinical Cancer Research (2015) 34:152 DOI: 10.1186/s13046-015-0270-2.
The impact of cyclin-dependent kinase 5 depletion on poly(ADPribose) polymerase activity and responses to radiation.
Bolin C, et al., Cell Mol Life Sci. 2011 Sept 16.
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SilenciX® is a registered trademark of tebu-bio; technology licensed from the Atomic Energy and Alternative Energies Commission (CEA). 
Interested in SilenciX® HeLa cells or custom cell lines?
In Europe, custom SilenciX cell lines and SilenciX HeLa cells are available via tebu-bio.
Contact Nadia Normand PhD (Business Development Manager) for any further assistance - nadia.normand @ tebu-bio.com
In United States of America and Canada:
LifeSensors - info @ lifesensors.com
In Japan:
Funakoshi - jutaku @ funakoshi.co.jp .jpg)
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