Literature DB >> 32647409

The Upregulation of hsa-mir-181b-1 and Downregulation of Its Target CYLD in the Late-Stage of Tumor Progression of Breast Cancer.

Alireza Andalib1, Shadi Rashed1, Moein Dehbashi2, Jamshid Hajati3, Farshid Noorbakhsh3, Mazdak Ganjalikhani-Hakemi1.   

Abstract

Some microRNAs are usually dysregulated in the cancers and influencing tumor behavior and progression. Hsa-miR-181b-1 and its target CYLD are involved in regulating the inflammatory pathways. This study aimed to investigate the expression levels of hsa-mir-181b-1 and CYLD in a cohort of breast tumor tissues and normal adjacent tissues to assess their association with breast cancer stages. A total number of 60 breast samples including cancerous and normal adjacent tissue specimens were collected. After pathological study, the expression of hsa-mir-181b-1 and CYLD were measured by qRT-PCR method. The hsa-mir-181b-1 expression level was significantly increased in breast tumor tissues compared to the controls. This increase was associated with the disease progression. Conversely, CYLD expression level was decreased in tumor samples compared to normal samples, significantly. ROC curve data added other prestigious information of hsa-mir-181b-1 and CYLD by defining cancer and healthy tissues with high specificity and sensitivity at a proposed cutoff point. Also, bioinformatic enrichment for the possible targets of mature sequence of "hsa-mir-181b-5p" was performed. Computational analysis showed the five most significant pathways including metabolic, cancer, calcium signaling, PI3K-Akt signaling and focal adhesion pathways which may be influenced by hsa-mir-181b-1. Thus, we suggested hsa-mir-181b-1 and CYLD might be involved in the pathogenesis of breast cancer and could be considered as two biomarkers for prediction, prognosis and diagnosis of the stages of the breast cancer. © Association of Clinical Biochemists of India 2019.

Entities:  

Keywords:  Breast cancer; CYLD; Expression level; Inflammation; hsa-mir-181b-1

Year:  2019        PMID: 32647409      PMCID: PMC7326880          DOI: 10.1007/s12291-019-00826-z

Source DB:  PubMed          Journal:  Indian J Clin Biochem        ISSN: 0970-1915


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