Long non-coding RNAs (lncRNAs) and their N6-methyladenosine (m6A) modifications play an essential role in tumorigenesis and cancer progression. This study was designed to explore the value of m6A-related lncRNAs in prognosis and therapeutic applications of immune infiltration of colon adenocarcinoma (COAD). We downloaded the COAD gene expression and clinical data from The Cancer Genome Atlas project. By co-expression analysis, Lasso Cox regression analysis, and univariate and multivariate Cox regression, we constructed an independent prognostic signature of seven m6A-related lncRNAs. The prognostic lncRNAs were divided into two clusters by consistent clustering analysis, as well as into two groups of low–high risk based on the signature. Then we identified the relationship between the different groups with clinical features and immune cell infiltration. Cluster 2 had a higher risk score with a lower survival rate. The risk score was higher in groups with advanced clinical features, such as stage III–IV, N1-3, and M1. The expression of AC156455.1 was increased in tumor tissues and cluster 2, and the lncRNA ZEB1−AS1 was notably higher in the high-risk group. Five types of immune cells showed differences in two clusters, and most were upregulated in type 2. The expression of memory B cells was positively correlated with the risk score. The prognostic model was verified by the Gene Expression Omnibus (GEO) dataset. Besides, we found that the expression of these seven lncRNAs in tumor tissues was significantly higher than that in normal tissues, which verified the feasibility of the model. Thus, the signature of seven m6A-related lncRNAs can independently predict the prognosis of COAD. This signature is also closely associated with immune cell infiltration, and new therapeutic targets can be explored from this field.

Breast cancer is the most common invasive cancer in women and the second leading cause of cancer death in women. However, it is not clear about its effective treatments. As a potential anticancer agent, grape seed procyanidins (GSPs) have been shown to inhibit the proliferation of various cancer cells in vitro and in vivo. In this study, it was shown that GSPs significantly inhibit MCF-7 cell proliferation in a concentration/time-dependent manner. The flow cytometric data clearly demonstrated that GSPs cause cell cycle arrest in the G2/M phase, followed by cell apoptosis. Moreover, it also confirmed that growth inhibition mediated by treatment with GSPs is related to the induction of apoptosis due to p53 elevation, purportedly by inhibition of the epidermal growth factor receptor (EGFR)/vascular endothelial growth factor (VEGF)/matrix metalloproteinase 9 (MMP9) pathway. Taken together, these findings suggest that GSPs inhibit MCF-7 cells proliferation and induce cell apoptosis by suppressing EGFR/VEGF/MMP9 pathway.