Bladder cancer is one of the most common malignant tumors in the urinary system. Among men, bladder cancer is the 6th most common cause of cancer and the 9th leading cause of cancer-related death. Currently, surgery is the main treatment for bladder cancer, but its recurrence rate and metastasis rate are high, which seriously affects the prognosis of patients. Therefore, it is necessary to further explore the molecular mechanism of bladder cancer in order to find effective drugs for the treatment of bladder cancer as soon as possible. CD BioSciences provides precise In Vivo transfection services of bladder cancer to assist in the study of the molecular functions of bladder cancer-related genes.

Target Genes Delivered In Vivo in Bladder Cancer

Through bioinformatics analysis, compared with normal tissues, genes such as TPM1, ACTC1, ACTA2, TPM2, TAGLN, CALD1, LMOD1, MYH11, and CNN1 were abnormally expressed in bladder cancer.

Figure 1. Cellular pathways affected in bladder cancer and targeting therapies. (an Kessel KE, et al.; 2015)

Studies have found that mutations of ACTC1 and TPM1 are closely related to the development of hypertrophic cardiomyopathy, mainly because ACTC1, ACTA2, TPM1, TPM2, and TAGLN all belong to the actin family, and actin is a highly conserved protein widely distributed in the biological world. Proteins that regulate cell proliferation, cell migration, and apoptosis, and cell protrusion mediated by actin assembly kinetics is a key step in cell invasion. TAGLN is an actin-binding protein and tumor suppressor factor, which has been reported to be involved in the occurrence and development of bladder cancer. TAGLN can inhibit the proliferation and invasion of bladder cancer cells in vitro, and inhibit tumorigenesis In Vivo. Although ACTA2, ACTC1, TPM1, TPM2, CALD1, LM-OD1, MYH11 and CNN1 have not been reported in bladder cancer, their carcinogenic effects have been confirmed in some tumors. The expression of ACTC1 is significantly up-regulated in glioblastoma, which can inhibit the migration of cancer cells. And ACTC1 is related to the prognosis of glioblastoma, and it can be used as a new type of prognostic marker in glioma. CALD1 is a cytoskeleton protein, and the up-regulation of 1-CAD expression caused by its mismatch can lead to abnormal angiogenesis in glioma. In addition, studies have found that LMOD1 can be used as a new gastric cancer biomarker and therapeutic target to induce EMT by regulating the FAKAkt/mTOR pathway. CNN1 plays a tumor suppressor role in breast cancer, as a downstream target of miR-106b-5p, its expression level is down-regulated in breast cancer tissues and cell lines, and it is negatively correlated with the expression of miR-106b-5p. miR-106b-5p can promote breast cancer cell carcinogenesis by targeting CNN1 and Rho/ROCK1 pathways.

In addition to the above genes, there are interesting bladder 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 bladder 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 Bladder cancer tissues and cells, and is toxic to the body;
• The In Vivo transfection system used cannot penetrate the Bladder 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 Bladder 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. SUNG H, et al.; Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwidefor 36 Cancers in 185 Countries. A: a Cancer Journal for Clini-cians. 2021,71(3):209-249.
2. DESPOND E A, DAWSON JF. Classifying Cardiac Actin MutationsAssociated With Hypertrophic Cardiomyopathy. Frontiers inPhysiology. 2018(9):405.
3. INSALL R. Actin in 202.Current biology: CB. 2021,31(10):496-498.
4. ASSINDER S J, et al.; Transgelin: an actin-binding protein and tumour suppressor. The International Journal of Biochemistry Cell Biology. 2009,41(3):482-486.
5. WANIBUCHI M, et al.; Actin, alpha, car-diac muscle 1 (ACTC1) knockdown inhibits the migration of glio-blastoma cells in vitro. Journal of The Neurological Sciences. 2018,39(2):117-121.
6. OHTAKI S, et al.; ACTC1 as an invasion and prognosis marker in glioma. Journal of Neurosurgery. 2017,126(2):467-475.
7. CHENG Q, et al.; CALD1 Modulates GliomasProgression via Facilitating Tumor Angiogenesis. Cancers. 2021,13(11):132-140.
8. van Kessel KE, et al.; Targeted therapies in bladder cancer: an overview of in vivo research. Nat Rev Urol. 2015, 12(12):681-94.

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