Cancer, the second leading cause of death globally, manifests through genomic instability, mutations, and non-mutational epigenetic alterations. Researchers have linked PRIM2, a subunit of the DNA polymerase α-primase complex that plays a role in DNA replication, to cancer progression. However, a comprehensive pan-cancer analysis has yet to be conducted.
The research team obtained PRIM2 gene expression data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) databases. They employed a variety of bioinformatics analysis tools to thoroughly investigate the associations between PRIM2 expression levels and clinical features, disease diagnosis, prognosis, cancer subtypes, immune regulation mechanisms, and drug sensitivity. In addition, they conducted validation experiments using the HT-29 and HepG2 cell lines to empirically verify the results of the bioinformatics analysis.
N Cadherin Antibody is a non-conjugated and Rabbit origined monoclonal antibody.
N-cadherin is one of the key proteins in the epithelial-mesenchymal transition (EMT) process. The overexpression of N-cadherin closely associates with the invasiveness and metastatic potential of tumors. By detecting the expression changes of N-cadherin, researchers can verify the role of PRIM2 in cell proliferation, migration, invasion, and EMT.
Figure 1. EMT-related protein expression in HepG2 and HT-29 cells with PRIM2 knockdown.
Researchers used N-cadherin antibody to conduct detection. The results of Western blot (WB) analysis showed the protein expression levels in HT-29 and HepG2 cell lines under PRIM2 gene knockdown conditions (using si-PRIM2-1 and si-PRIM2-3 interference sequences) and control conditions (using si-NC negative control sequence). These results indicated that once the PRIM2 gene was effectively knocked down, the expression level of N-cadherin noticeably declined. This finding implies that a lack of PRIM2 can impede the EMT process. In addition, the expression of the epithelial marker ZO-1 went up. This increase provides more evidence that PRIM2 knockdown can inhibit EMT. Overall, these results highlight the crucial role of PRIM2 in regulating EMT and its potential as a therapeutic target.
Reference
[1] Xi Z. et al; Wiley International Journal of Genomics Volume 2024, Article ID 8834415, 31 pages.
