Difference between revisions of "Part:BBa K3063902"
Samsoncheung (Talk | contribs) |
|||
| (One intermediate revision by one other user not shown) | |||
| Line 3: | Line 3: | ||
<partinfo>BBa_K3063902 short</partinfo> | <partinfo>BBa_K3063902 short</partinfo> | ||
| − | The part encodes artificial microRNA (amiRNA) that silences SOX4, a gene conferring cancer stem cell (CSC) properties. SOX4-targeting amiRNA in the transformed salmonella, will form dsRNA upon binding to stemness SOX4 mRNA in tumour cells. Under the aid of this particular biobrick, RNA silencing and degradation of SOX4 mRNA in liver cancer stem cells can be achieved simultaneously. | + | The part encodes artificial microRNA (amiRNA) that silences SOX4, a gene conferring cancer stem cell (CSC) properties. <ref> Qi, M., Hu, J., Cui, Y., Jiao, M., Feng, T., Li, X., ... & Zhang, H. (2019). CUL4B promotes prostate cancer progression by forming positive feedback loop with SOX4. Oncogenesis, 8(3), 23. </ref> SOX4-targeting amiRNA in the transformed salmonella, will form dsRNA upon binding to stemness SOX4 mRNA in tumour cells. Under the aid of this particular biobrick, RNA silencing and degradation of SOX4 mRNA in liver cancer stem cells can be achieved simultaneously. |
<!-- Add more about the biology of this part here | <!-- Add more about the biology of this part here | ||
| Line 30: | Line 30: | ||
===Part Therapeutics=== | ===Part Therapeutics=== | ||
| − | Evidence has been accumulating that SOX4, whose expression initiated by STAT3, orchestrates epithelIal-to-mesenchymal transition (EMT) through upregulating a series of EMT-inducing transcription factors, which then enhances | + | Evidence has been accumulating that SOX4, whose expression initiated by STAT3, orchestrates epithelIal-to-mesenchymal transition (EMT) through upregulating a series of EMT-inducing transcription factors, which then enhances cellular growth as well as transformation. <ref> Lourenço, A. R., & Coffer, P. J. (2017). SOX4: joining the master regulators of epithelial-to-mesenchymal transition?. Trends in cancer, 3(8), 571-582. </ref> For instance, SOX4 is associated with cell survival in tumour population growth, as well as the metastatic properties of the in vitro <ref> Grimm, D., Bauer, J., Wise, P., Krüger, M., Simonsen, U., Wehland, M., … Corydon, T. J. (2019). The role of SOX family members in solid tumours and metastasis. Seminars in Cancer Biology. doi: 10.1016/j.semcancer.2019.03.004 </ref>. SOX4 knockdown can effectively reduce the activation of transforming growth factor-beta (TGF-β) signalling, attenuating the invasion of cancer cells. <ref> Foronda, M., Martínez, P., Schoeftner, S., Gómez-López, G., Schneider, R., Flores, J. M., ... & Blasco, M. A. (2014). Sox4 links tumor suppression to accelerated aging in mice by modulating stem cell activation. Cell reports, 8(2), 487-500. </ref> |
=References= | =References= | ||
Latest revision as of 02:54, 22 October 2019
eSIBR construct fragment for SOX4
The part encodes artificial microRNA (amiRNA) that silences SOX4, a gene conferring cancer stem cell (CSC) properties. [1] SOX4-targeting amiRNA in the transformed salmonella, will form dsRNA upon binding to stemness SOX4 mRNA in tumour cells. Under the aid of this particular biobrick, RNA silencing and degradation of SOX4 mRNA in liver cancer stem cells can be achieved simultaneously.
Sequence and Features
- 10COMPATIBLE WITH RFC[10]
- 12COMPATIBLE WITH RFC[12]
- 21INCOMPATIBLE WITH RFC[21]Illegal XhoI site found at 156
- 23COMPATIBLE WITH RFC[23]
- 25COMPATIBLE WITH RFC[25]
- 1000COMPATIBLE WITH RFC[1000]
Introduction
Biology
Part structure
The part for SOX4 silencing in cancer stem cells
BBa_K3063902 The BioBrick encodes SOX4 targeting amiRNA. With the help of enhanced enhanced synthetic inhibitory BIC/miR-155 RNA (eSIBR) vector, pri-miRNA hairpin as shown below is transcribed and later processed into mature miRNA in Salmonella Typhimurium that achieve SOX4 knockdown in target cancer cells.
Part Therapeutics
Evidence has been accumulating that SOX4, whose expression initiated by STAT3, orchestrates epithelIal-to-mesenchymal transition (EMT) through upregulating a series of EMT-inducing transcription factors, which then enhances cellular growth as well as transformation. [2] For instance, SOX4 is associated with cell survival in tumour population growth, as well as the metastatic properties of the in vitro [3]. SOX4 knockdown can effectively reduce the activation of transforming growth factor-beta (TGF-β) signalling, attenuating the invasion of cancer cells. [4]
References
- ↑ Qi, M., Hu, J., Cui, Y., Jiao, M., Feng, T., Li, X., ... & Zhang, H. (2019). CUL4B promotes prostate cancer progression by forming positive feedback loop with SOX4. Oncogenesis, 8(3), 23.
- ↑ Lourenço, A. R., & Coffer, P. J. (2017). SOX4: joining the master regulators of epithelial-to-mesenchymal transition?. Trends in cancer, 3(8), 571-582.
- ↑ Grimm, D., Bauer, J., Wise, P., Krüger, M., Simonsen, U., Wehland, M., … Corydon, T. J. (2019). The role of SOX family members in solid tumours and metastasis. Seminars in Cancer Biology. doi: 10.1016/j.semcancer.2019.03.004
- ↑ Foronda, M., Martínez, P., Schoeftner, S., Gómez-López, G., Schneider, R., Flores, J. M., ... & Blasco, M. A. (2014). Sox4 links tumor suppression to accelerated aging in mice by modulating stem cell activation. Cell reports, 8(2), 487-500.