miR-17-92a-1 cluster host gene: a key regulator in colorectal cancer development and progression.

Colorectal cancer (CRC), recognized among the five most prevalent malignancies and most deadly cancers, manifests multifactorial influences stemming from environmental exposures, dietary patterns, age, and genetic predisposition. Although substantial progress has been made in comprehending the etiology of CRC, the precise genetic components driving its pathogenesis remain incompletely elucidated. Within the expansive repertoire of non-coding RNAs, particular focus has centered on the miR-17-92a-1 cluster host gene (MIR17HG) and its associated miRNAs, which actively participate in diverse cellular processes and frequently exhibit heightened expression in various solid tumors, notably CRC. Therefore, the primary objective of this research is to undertake an extensive inquiry into the regulatory mechanisms, structural features, functional attributes, and potential diagnostic and therapeutic implications associated with this cluster in CRC. Furthermore, the intricate interplay between this cluster and the development and progression of CRC will be explored. Our findings underscore the upregulation of the miR-17-92a-1 cluster host gene (MIR17HG) and its associated miRNAs in CRC compared to normal tissues, thus implying their profound involvement in the progression of CRC. Collectively, these molecules are implicated in critical oncogenic processes, encompassing metastatic activity, regulation of apoptotic pathways, cellular proliferation, and drug resistance. Consequently, these findings shed illuminating insights into the potential of MIR17HG and its associated miRNAs as promising targets for therapeutic interventions in the management of CRC.

Cellular senescence molecules expression in type 2 diabetes mellitus: CDKN2A, CDKN2B, and lncRNA ANRIL.

AIMS: Cellular senescence in type 2 diabetes mellitus (T2DM) has received widespread attention. However, the cellular senescence molecules involved in T2DM are unclear. Furthermore, there are no consistent biomarkers for cellular senescence in T2DM. Therefore, this study aimed to identify cellular senescence molecules in T2DM and investigate their expression in peripheral blood mononuclear cells of individuals with T2DM. METHODS: Patients with T2DM (n = 40) and healthy controls (n = 40) were enrolled. We used different databases to identify cellular senescence molecules in T2DM and confirmed the obtained genes and lncRNA using real-time PCR. RESULTS: Bioinformatics analysis indicated that CDKN2A and CDKN2B genes, and long noncoding RNA ANRIL are the most effective cellular senescence molecules in T2DM. Furthermore, CDKN2A and ANRIL expression decreased in individuals with T2DM. CONCLUSIONS: Cellular senescence may have a protective effect against T2DM. In addition, the cellular senescence molecules CDKN2A and ANRIL may be potential biomarkers of cellular senescence in T2DM.