N6-methyladenosine of TRIM27 enhances the stem cell-type phenotype of cisplatin-resistant colorectal cancer cells.

Colorectal cancer (CRC), classified as a lethal form of cancer, substantially threatens human well-being. Cancer stem cells (CSCs) reflect subsets for cancerous cells having basic stem-cell type properties, being significantly involved in the development of chemoresistance and tumor relapsing. The aberrant TRIM27 expression in various types of cancer indicates its potential involvement in cancer growth and progression. The current understanding of the TRIM27 involvement in CRC remains limited. In current study indicated that TRIM27 can potentially promote CSC-type phenotype of Cisplatin (DDP)-resistant CRC cells. YTHDF1 recruitment onto m6A-amended TRIM27 was crucial for facilitating the TRIM27 translating process in DDP-resistant CRC cells. The present research proposes that TRIM27 exhibits an oncogenic role by enhancing the CSC-type properties in DDP-resistant CRC via the m6A-modified pathway. The potential therapy for combating the relapse of CRC may include TRIM27 and YTHDF1, as they have been found to have significant roles in promoting CSC-type phenotypic characteristics.

miRNA-425-5p enhances diffuse large B cell lymphoma growth by targeting PTEN.

BACKGROUND: At present, cancer is one of the greatest threats to mankind, and is associated with the highest rates of morbidity and comorbidity. Recently, the advancements in molecular biology have led to an in-depth understanding of the underlying pathophysiology, which may further impact the lead time in the context of early discovery and effective therapy of cancer. Therefore, the present study proposes a better understanding of the role of micro(miR)-425-5p in diffuse large B-cell lymphoma (DLBC). METHODS: qRT-PCR was carried out to detect the relevant proteins, miRNA and mRNA RNA gene expression in DLBC cells. The effect of miR-425-5p on DLBC growth was examined by CCK-8 and colony formation assays. The binding relationship between genes was verified by dual-luciferase reporter gene assay. RESULTS: We demonstrated how the over-expression of miR-425-5p can lead to increased progression of DLBC by increasing the cellular proliferation rate and colony-forming ability. Additionally, we also found that the expression of miR-425-5p could be significantly inhibited on the basis of phosphatase and tensin homolog (PTEN) signaling pathways. CONCLUSIONS: The present study concludes that miR-425-5p is responsible for the oncogenic progression and relapse of DLBC tumorigenesis via PTEN/PI3K signaling, which can thus be effectively used to achieve better therapeutic outcomes.

Single nucleotide polymorphisms within the Wnt pathway predict the risk of bone metastasis in patients with non-small cell lung cancer.

The Wingless-type (Wnt) signaling pathway plays an important role in the development and progression of cancer. This study aimed to evaluate the relationship between single nucleotide polymorphisms (SNPs) in the Wnt pathway and the risk of bone metastasis in patients with non-small cell lung cancer (NSCLC). We collected 500 blood samples from patients with NSCLC and genotyped eight SNPs from four core genes (WNT2, AXIN1, CTNNB1 and APC) present within the WNT pathway. Moreover, we assessed the potential relationship of these genes with bone metastasis development. Our results showed that the AC/AA genotype of CTNNB1: rs1880481 was associated with a decreased risk of bone metastasis. Polymorphisms with an HR of < 1 had a cumulative protective impact on the risk of bone metastasis. Furthermore, patients with the AC/AA genotype of CTNNB1: rs1880481 was associated with Karnofsky performance status score, squamous cell carcinoma antigen and Ki-67 proliferation index. Lastly, patients with the AC/AA genotype of CTNNB1: rs1880481 had significantly longer median progression free survival time than those with the CC genotype. In conclusion, SNPs within the Wnt signaling pathway are associated with a decreased risk of bone metastasis, and may be valuable biomarkers for bone metastasis in patients with NSCLC.

miR-192/215-5p act as tumor suppressors and link Crohn's disease and colorectal cancer by targeting common metabolic pathways: An integrated informatics analysis and experimental study.

MicroRNAs have emerged as key regulators involved in a variety of biological processes. Previous studies have demonstrated that miR-192/215 participated in progression of Crohn's disease and colorectal cancer. However, their concrete relationships and regulation networks in diseases remain unclear. Here, we used bioinformatics methods to expound miR-192/215-5p macrocontrol regulatory networks shared by two diseases. For data mining and figure generation, several miRNA prediction tools, Human miRNA tissue atlas, FunRich, miRcancer, MalaCards, STRING, GEPIA, cBioPortal, GEO databases, Pathvisio, Graphpad Prism 6 software, etc . are extensively applied. miR-192/215-5p were specially distributed in colon tissues and enriched biological pathways were closely associated with human cancers. Emerging role of miR-192/215-5p and their common pathways in Crohn's disease and colorectal cancer was also analyzed. Based on results derived from multiple approaches, we identified the biological functions of miR-192/215-5p as a tumor suppressor and link Crohn's disease and colorectal cancer by targeting triglyceride synthesis and extracellular matrix remodeling pathways.