Prostate cancer (PCa) is one of the most common cancers in men and ranks second in incidence among male malignancies worldwide. Therefore, there is an urgent need for new and efficient therapeutic drugs in clinical treatment. However, the development of highly effective drug therapies is based on a deep understanding of the molecular mechanisms and functions of prostate cancer. To this end, we have developed an in vivo delivery transfection system specifically for prostate cancer to help in-depth study of its related genes.

Target Genes Delivered In Vivo in Prostate Cancer

Through bioinformatics analysis, 14 key genes (P4HB, ERGIC1, FOXA1, RP11-498C9.2, HNRNPF, CANT1, SYNGR2, HID1, EIF2AK1, MARCKSL1, NME1, ST14, HPN, RAB3D) related to PCa patients have been discovered so far, and compared with normal paracancerous tissues, they were all highly expressed in PCa tissues. Among them, P4HB is an autophagy-related gene. Autophagy can both inhibit and promote tumors. Under normal circumstances, it can inhibit the canceration of cells in the early stage of tumors, but after the formation of tumors, autophagy will maintain and promote the development of tumors. Previous studies have found that high expression of P4HB is also found in PCa tissues. Will downregulation of P4HB affect the development of PCa remains to be studied. Abnormal expression of ERGIC1, a circulating membrane protein closely associated with the endoplasmic reticulum, can lead to endoplasmic reticulum dysfunction, which in turn may affect cancer cells, for example, endoplasmic reticulum stress (ERS) disorders may occur, while Tumors will undergo changes such as inhibition or proliferation according to the different regulatory effects of ERS. ERGIC1 has different effects on different tumors. Low expression may promote the occurrence and progression of gastric cancer, but silencing ERGIC1 in PCa can inhibit tumors. RP11-498C9.2 is a member of the RP11 family. Different members of the family have different effects on malignant tumors. Upregulation of RP11-468E2.5 can inhibit the proliferation of colorectal cancer cells, and downregulation of RP11-295G20.2 can inhibit the proliferation of hepatocellular carcinoma in vivo. growth, and knockdown of RP11-567G11.1 attenuated the proliferation and invasion of renal cell carcinoma cells. However, in the bioinformatics analysis, it was found that RP11-498C9. 2 was also highly expressed in PCa tissues, and the specific mechanism needs to be further analyzed. HNRNPF belongs to the subfamily of heterogeneous nuclear ribonucleoproteins (hnRNPs), which play important roles in gene expression and signal transduction. Studies found that hnRNPs are associated with cancer, so HNRNPF may also be related to carcinogenesis. Some studies have found that HNRNPF is overexpressed in glioma and bladder cancer. Knocking down HNRNPF can inhibit the proliferation of glioma and bladder cancer cells. HNRNPF is also related to PCa and is highly expressed in PCa. Rab3D, one of the Rab3 isoforms that are oncogenic in breast, colon, esophageal, skin and brain tumors, upregulation of Rab3D promotes tumor cell proliferation. HID1 encodes a transport-related protein. Studies have found that HID1 is associated with non-functioning pituitary adenomas, and its expression is lost in breast, cervical, lung, thyroid, and gastrointestinal cancer cell lines. EIF2AK1 is an EIF2S1 kinase that mediates EIF2S1 phosphorylation and is associated with endometrial carcinogenesis. SYN GR2 is a member of the synaptoencephalin family and may be involved in the distinction between benign and malignant thyroid tumors. Studies have found that FOXA1, CANT1, MARCKSL1, NME1, HPN, and ST14 are related to the pathogenesis and progression of PCa, and participate in different mechanisms to affect the occurrence and development of PCa. The relationship is still unclear and needs to be further explored.

Figure 1. Gene therapy treatment approaches in humans: direct tumour injection and vaccine-based systemic injection. (Gregg JR,et al.; 2021)

In addition to the above genes, there are interesting prostate 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 prostate 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 prostate cancer tissues and cells, and is toxic to the body;
• The in vivo transfection system used cannot penetrate the prostate 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 prostate 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.

Reference

1. WANG F R, et al.; Aberrant DNA-PKcs and ERGIC1 expression may be involved in initiation of gastric cancer. World J Gastroenterol. 2017, 23(33): 6119-6127.
2. JIANG L, et al.; Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6. J Exp Clin Cancer Res. 2019, 38(1): 465.
3. JIANG L, et al.; Long non-coding RNA RP11-468E2.5 curtails colorectal cancer cell proliferation and stimulates apoptosis via the JAK/STAT signaling pathway by targeting STAT5 and STAT6. J Exp Clin Cancer Res. 2019, 38(1): 465.
4. RAFFANIELLO R D. Rab3 proteins and cancer：Exit strategies. J Cell Biochem. 2021, 122(10): 1295-1301.

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