The independent effects of metastasis-promoting gene CD151 in the process of metastasis are not known. This study aimed to isolate CD151 to discover what its role in metastasis would be uninfluenced by potential interactions with other components and pathways in human cells. Results showed that CD151 significantly increased the adhesion of the cells and decreased their motility. Thus, it may be that CD151 is upregulated in cancer cells for the last step of metastasis, and it increases the chances of success of metastasis by aiding in implantation of the cancer cells. Targeting CD151 in chemotherapeutic modalities could therefore potentially slow or prevent metastasis.
Here, seeking to better understand the genetic associations underlying non-small cell lung cancer, the authors screened hundreds of genes, identifying that KCNMB2 upregulation was significantly correlated with poor prognoses in lung cancer patients. Based on this, they used small interfering RNA to decrease the expression of KCNMB2 in A549 lung cancer cells, finding decreased cell proliferation and increased lung cancer cell death. They suggest this could lead to a new potential target for lung cancer therapies.
Treatments inhibiting Notch signaling pathways have been explored by researchers as a new approach for the treatment of glioblastoma tumors, which is a fast-growing and aggressive brain tumor. Recently, retinoic acid (RA) therapy, which inhibits Notch signaling, has shown a promising effect on inhibiting glioblastoma progression. RA, which is a metabolite of vitamin A, is very important in embryonic cellular development, which includes the regulation of multiple developmental processes, such as brain neurogenesis. However, high doses of RA treatment caused many side effects such as headaches, nausea, redness around the injection site, or allergic reactions. Therefore, we hypothesized that a combination treatment of RA and siRNA targeting NOTCH1 (siNOTCH1), the essential gene that activates Notch signaling, would effectively inhibit brain cancer cell proliferation. The aim of the study was to determine whether inhibiting NOTCH1 would inhibit the growth of brain cancer cells by cell viability assay. We found that the combination treatment of siNOTCH1 and RA in low concentration effectively decreased the NOTCH1 expression level compared to the individual treatments. However, the combination treatment condition significantly decreased the number of live brain cancer cells only at a low concentration of RA. We anticipate that this novel combination treatment can provide a solution to the side effects of chemotherapy.
Here, the authors chose to investigate the efficacy of zinc oxide nanoparticles (ZnO NPs) and cisplatin or zinc ions in inducing cancer apoptosis. While both treatments were found to reduce the proliferation of lung cancer cells, the authors suggest that further studies to identify the mechanism are necessary.
In this study, we aimed to characterize CD44-mediated regulation of the Wnt/β-catenin signaling pathway, which promotes cancer invasion and metastasis. We hypothesized that CD44 down-regulation will inhibit gastric cancer cell migration and invasion by leading to down-regulation of Wnt/β-catenin signaling. We found that CD44 up-regulation was significantly related to poor prognosis in gastric cancer patients. We demonstrated the CD44 down-regulation decreased β-catenin protein expression level. Our results suggest that CD44 down-regulation inhibits cell migration and invasion by down-regulating β-catenin expression level.
Pancreatic cancer is one of the deadliest cancers, with a 10% 5-year survival rate. The authors studied various dosages of TPEN and zinc in combination with Chloroquine and Gemcitabine as treatments to reduce cell proliferation. Results showed that when combined with Chloroquine and Gemcitabine, zinc and TPEN both significantly lowered cell proliferation compared to Gemcitabine, suggesting a synergistic effect that resulted in a more cytotoxic treatment. Further research and clinical trials on this topic are needed to determine whether this could be a viable treatment for pancreatic cancer.
Uveal melanoma (UM) is a rare subtype of melanoma but the most frequent primary cancer of the eye in adults. The goal of this study was to research the genetic causes of UM through a comprehensive frequency analysis of base-pair mismatches in patient genomes. Results showed a total of 130 genetic mutations, including seven recurrent mutations, with most mutations occurring in chromosomes 3 and X. Recurrent mutations varied from 8.7% to 17.39% occurrence in the UM patient sample, with all mutations identified as missense. These findings suggest that UM is a recessive heterogeneous disease with selective homozygous mutations. Notably, this study has potential wider significance because the seven genes targeted by recurrent mutations are also involved in other cancers.
In the United States, there are currently 17.8 million affected by atopic dermatitis (AD), commonly known as eczema. It is characterized by itching and skin inflammation. AD patients are at higher risk for infections, depression, cancer, and suicide. Genetics, environment, and stress are some of the causes of the disease. With the rise of personalized medicine and the acceptance of gene-editing technologies, AD-related variations need to be identified for treatment. Genome-wide association studies (GWAS) have associated the Filaggrin (FLG) gene with AD but have not identified specific problematic single nucleotide polymorphisms (SNPs). This research aimed to refine known SNPs of FLG for gene editing technologies to establish a causal link between specific SNPs and the diseases and to target the polymorphisms. The research utilized R and its Bioconductor packages to refine data from the National Center for Biotechnology Information's (NCBI's) Variation Viewer. The algorithm filtered the dataset by coding regions and conserved domains. The algorithm also removed synonymous variations and treated non-synonymous, frameshift, and nonsense separately. The non-synonymous variations were refined and ordered by the BLOSUM62 substitution matrix. Overall, the analysis removed 96.65% of data, which was redundant or not the focus of the research and ordered the remaining relevant data by impact. The code for the project can also be repurposed as a tool for other diseases. The research can help solve GWAS's imprecise identification challenge. This research is the first step in providing the refined databases required for gene-editing treatment.
The authors looked at whether traditional Chinese medicine remedies that target the lungs and liver would reduce inflammation in a planaria model. They found that the two active compounds they tested were able to decrease induced inflammation by 97-98%.
