Astrocytoma refers to the tumor formed by astrocytes, accounting for 13% to 26% of intracranial tumors, accounting for 21.2% to 51.6% of gliomas, and more men than women. Astrocytic tumors can occur in any part of the central nervous system. Generally, they are more common in the cerebral hemispheres and subthalamic ganglia in adults, and more common in children in the infratentorial area. Astrocytoma is an invasive growth tumor, and most tumors may recur after resection, and the tumor may evolve into anaplastic astrocytoma or glioblastoma multiforme after recurrence. Therefore, it is necessary to further explore the molecular mechanism of Astrocytoma in order to find effective drugs for the treatment of Astrocytoma as soon as possible. CD BioSciences provides precise in vivo transfection services of astrocytoma to assist in the study of the molecular functions of astrocytoma-related genes.

Target Genes Delivered in vivo in Astrocytoma

Through bioinformatics analysis, compared with normal tissues, genes such as Id3、PRSS11、SPOCK2、SORL1, and APOD were abnormally expressed in astrocytoma.

Figure 1.13-year-old female with a diffuse anaplastic astrocytoma of the left basal ganglia. (Zaccagna F, et al.; 2021)

Id gene encodes a protein that interferes with transcriptional activation and is required to maintain vasculature invasiveness for neuronal differentiation and angiogenesis. Id3 protein has previously been demonstrated in endothelial cells of astrocytic tumor vessels, and its expression correlates with tumor vascularity.

PRSS11 encodes the serine protease HtrA1, a candidate tumor suppressor involved in protease-induced cell death. Downregulation of PRSS11 has been observed during progression of ovarian cancer as well as melanoma. Furthermore, microarray analysis of metastatic melanoma cells found downregulation of PRSS11 compared with non-metastatic melanoma cells, and overexpression of PRSS11 led to suppression of melanoma growth. Differential expression of PRSS11 was also observed between highly migratory U373MG glioma cells compared with slower migrating primary glioblastoma cells.

KIAA0275 (SPOCK2, testican 2) encodes a calcium-binding proteoglycan expressed primarily in the brain, but so far little information is available on its function. SPOCK2 was recently shown to abrogate the inhibition of MT1- or MT3-MMP-mediated pro-MMP-2 activation by other testis family members. This appears to be counterproductive in promoting protease-mediated invasion. However, in previous studies, it was found that the expression levels of all testicular family members in astrocytomas decreased with increasing tumor grade. These findings appear to indicate another function of SPOCK2, which is currently unknown. SORL1 (SorLA/LR11) encodes a member of the LDL receptor superfamily that is ubiquitously expressed in the nervous system and functions as a neuronal apolipoprotein E receptor. Unlike other downregulated genes, the link between SORL1 and tumor progression has not been proven. A marked and consistent loss of LR11 protein in histologically normal-appearing neurons was observed in Alzheimer's disease patients. LR11 has also been shown to interact with the plasminogen activation system and PDGF-BB signaling, which has potential implications for astrocytoma progression.

APOD encodes a human plasma protein, apolipoprotein D, which belongs to the apolipoprotein superfamily. Results of the study showed that APOD was downregulated in all age groups with malignant astrocytoma and that APOD is a proven marker of low-grade, non-invasive astrocytoma. Furthermore, in human breast cancer cells, increased APOD expression was accompanied by inhibition of cell proliferation and progression through a more differentiated phenotype. Likewise, apo-D secretion was inversely correlated with cell proliferation and cell density in human prostate cancer cells.

In addition to the above genes, there are interesting astrocytoma-related genes that need to be explored and studied. Therefore, there is a need for an in vivo transfection system that can precisely target astrocytoma 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 Astrocytoma tissues and cells, and is toxic to the body;
• The in vivo transfection system used cannot penetrate the Astrocytoma 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 Astrocytoma 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. Komotar RJ, et al.; Pilomyxoid astrocytoma: a review. MedGenMed. 2004, 6(4):42.
2. Salles D, et al.; Pilocytic Astrocytoma: A Review of General, Clinical, and Molecular Characteristics. J Child Neurol. 2020, 35(12):852-858.
3. Hirtz A, et al.; Astrocytoma: A Hormone-Sensitive Tumor? Int J Mol Sci. 2020, 21(23):9114.
4. MacDonald TJ, et al.; Progression-associated genes in astrocytoma identified by novel microarray gene expression data reanalysis. Methods Mol Biol. 2007, 377:203-22.
5. Zaccagna F, et al.; Imaging and treatment of brain tumors through molecular targeting: Recent clinical advances. Eur J Radiol. 2021,142:109842.

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