Cervical cancer is one of the most common malignant tumors in women all over the world. Its mortality rate is increasing year by year and its incidence is younger, which seriously threatens women's health. Although the surgical treatment of cervical cancer is becoming more and more mature, it has not achieved satisfactory curative effect for advanced patients. Therefore, it is necessary to further explore the molecular mechanism of cervical cancer in order to find effective drugs for the treatment of cervical cancer as soon as possible. CD BioSciences provides precise in vivo transfection services for cervical cancer tissues to assist in research on the molecular functions of cervical cancer-related genes.

Target Genes Delivered in vivo in Cervical Cancer

Through years of continuous development and research of molecular biology techniques, VEGF, EGFR, mTOR, HDAC, COX-2, MMPs and other mutant genes have been discovered in Cervical Cancer

Figure 1. miRNAs as a therapeutic target against cervical cancer. (Áyen Á, et al.; 2020)

Vascular Endothelial Growth Factor Inhibitor (VEGF)

VEGF is a secreted glycoprotein that specifically stimulates vascular endothelial cell proliferation, migration and vascular remodeling in a paracrine and autocrine manner after binding to tyrosine kinase receptors, and is essential for tumor growth and metastasis. Study found that the expression level of VEGF mRNA was significantly positively correlated with the clinicopathological stage, pathological differentiation degree, lymph node metastasis, tumor diameter and deep myometrial invasion of cervical cancer. Therefore, VEGF and its receptors have become the main targets of anti-tumor therapy.

Epidermal Growth Factor Receptor (EGFR)

EGFR is a transmembrane glycoprotein that can activate tyrosine kinases, control cell division and proliferation, promote angiogenesis and tumor metastasis, and is closely related to the formation and development of tumors. Studies have found that EGFR is overexpressed in cervical cancer tissues. EGFR was the first growth factor receptor to be targeted for tumor therapy. EGFR antagonists are divided into anti-EGFR monoclonal antibodies and EGFR small molecule tyrosine kinase inhibitors (TKIs), both of which can inhibit tumor cell proliferation and induce cancer cell apoptosis by inhibiting EGFR autophosphorylation and downstream signal transduction.

mTOR

Mammalian target of rapamycin (mTOR) can regulate tumor growth and cell proliferation, participate in protein synthesis, and is the main target of PI3K/Akt pathway. Aberrant activation of mTOR contributes to many tumorigenesis, and dysregulation of its signaling pathway contributes to tumor cell proliferation and survival of cervical cancer cells. It has been observed that the mTOR signaling pathway is activated in cervical cancer.  Therefore, mTOR can also be used as the main target for anti-cervical cancer therapy.  In addition, there are many genes related to the apoptosis signaling pathway in the human body, such as p53, bcl-2, mdm-2 genes, etc., which are also good therapeutic targets for the treatment of cervical cancer.

HDAC

Histone deacetylase (HDAC) is a class of proteases related to the regulation of gene expression and structural modification of chromosomes. The acetylation of histone is beneficial to the dissociation of DNA and histone octamer, and the relaxation of nucleosome structure, so that various transcription factors and cooperative transcription factors can specifically bind to DNA binding sites and activate gene transcription. In the nucleus, the process of histone acetylation and histone deacetylation is in a dynamic balance, and is jointly regulated by histone acetyltransferase (histone acetyltransferase, HAT) and HDAC. Studies have found that HDAC inhibitors can induce the accumulation of acetylated histones in the chromatin P21WAF1 gene of cervical cancer cells, and inhibit the expression of malignant phenotype genes associated with cervical cancer cell lines.

In addition to the above genes, there are interesting cervical cancer-related genes that need to be explored and studied. Therefore, there is a need for an in vivo transfection system that can precisely target Cervical cancer tissue and be taken up by tumor cells to function in vivo. The system can help researchers overcome various challenges encountered during in vivo transfection:

• Relevant molecular function studies can only be carried out in vitro, lacking important in vivo data
• Using in vitro transfection system for in vivo transfection, the transfection efficiency is very low;
• The in vivo transfection system used is not specific to cervical cancer tissues and cells, and is toxic to the body;
• The in vivo transfection system used cannot penetrate the cervical cancer tissue into the tumor tissue;
• The nucleic acid load of the in vivo transfection system is low, and it is difficult to achieve the expected effect;
• Etc…

Our Advantage:

• We can provide an in vivo transfection system for cervical cancer tissues and cells to achieve efficient transfection
• Our system can target multiple targets at the same time, improving targeting accuracy
• The in vivo transfection system has low toxicity to the body and is safe to use
• In vivo transfection system vectors can protect nucleic acids from degradation during in vivo delivery
• Persistent knockout effect in experimental animals after a single injection
• The system load is high, and the transfection needs of different doses can be completed
• Professional design and service team to provide you with reliable service and technical support
• Timely feedback of technical reports

CD BioSciences specializes in developing transfection systems and customizing transfection reagents for gene transfection using our core technologies. With our high-quality products and services, your transfection results can be greatly improved. If you can't find a perfect in vivo transfection system, you can contact us. We can provide one-to-one personal customization service.

References

1. TOMAO F, et al.; Angiogenesis and antiangiogenic agents in cervical cancer. Onco Targets Ther. 2014, 7: 2237-2248.
2. SHI Y, et al.; Aquaporin 8 involvement in human cervical cancer SiHaMigration via the EGFR-Erk1 /2 pathway. Asian Pac J Cancer Prev. 2014,15(15): 6391-6395.
3. KANG S, et al.; Thioridazine induces apoptosis by targeting the PI3K/Akt /mTOR pathway in cervical and endometrial cancer cells. Apoptosis. 2012,17(9): 989-997.
4. HUI L, XINXING W．Histone deacetylase inhibitor,Trichostatin A,activates p21WAF1 /CIP1 expression through downregulation of c-myc and release of the repression of c-myc from the promoter in human cervical cancer cells. Biochem Biophys Res Commun. 2004, 324(2): 860-867．
5. Áyen Á, et al.; Targeted Gene Delivery Therapies for Cervical Cancer. Cancers (Basel). 2020, 12(5):1301.

* For research use only. Not for use in clinical diagnosis or treatment of humans or animals.