The SK-N-SH cell line was established in 1970 from the bone marrow metastasis of a 4-year-old female with neuroblastoma. SK-N-SH cells exhibit an epithelial morphology and adherent cultural properties. SK-N-SH is capable of differentiating and exhibiting neurite outgrowths. This hyperdiploid cell line has a modal chromosome number of 47 and is genetically female with two X chromosomes. SK-N-SH cells express blood type A and Rh+ , as well as produce high levels of dopamine-beta-hydroxylase.
Pediatric brain cancer is one of the leading causes of cancer-related deaths in children under 20 years old, and neuroblastoma cell lines like SK-N-SH are valuable tools in preclinical research that allow scientists to develop new drugs and treatments. A pre-optimized SK-N-SH transfection reagent to transfect SK-N-SH cells and conduct brain cancer research is commercially available from Altogen Biosystems. SK-N-SH cells can also be used to study neural pathways.
Past studies have shown that reducing miR-21 in breast, gastric, and colon cancer cell lines negatively affects tumor growth; however, the effects of reducing miR-21 in neuroblastoma cell lines had not yet been investigated. In a 2017 Oncology Letters study written by Wang et al., researchers use transfection methods to investigate how reducing microRNA (miR-21) affects SK-N-SH neuroblastoma cells. MicroRNA (miR-21) is an oncogenic version of miRNA, which is a short non-coding RNA that plays an important role in cell migration, proliferation, and differentiation. Researchers transfected an miR-21 inhibitor oligonucleotide into an SK-N-SH cell line. Quantitative polymerase chain reaction analysis and Western blotting analysis were used to detect the expression of miR-21 and examine the levels of PTEN, PDCD4 and caspase-3 proteins. Results revealed that the miR-21 inhibitor inhibited SK-N-SH cell proliferation and induced apoptosis. The miR-21 inhibitor also led to a significant increase of proteins PTEN and PDCD4 in SK-N-SH cells. Moreover, a control group with SK-N-SH cells that were not transfected with the miR-21 inhibitor showed an increase in caspase-3 protein expression. These findings suggest that miR-21 can serve as a novel therapeutic target in the treatment of neuroblastoma patients.
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