Studying the Expression of miR-1, EVI1 and Calreticulin in Invasive Breast Carcinoma: Relationship with Clinicopathological Parameters
Year: 2025
Type: article
Study design: Observational Study
Abstract: .Introduction: Breast cancer is the most prevalent cause of cancer-related mortality among women, with significant rates of morbidity and mortality. Although breast cancer is conventionally treated using various methods including surgery, chemotherapy and endocrine therapy , recurrence and metastasis still remain a serious issue in advanced stage patients. So, new therapeutic strategies are awfully needed.Objectives : In this research we tended to determine the expression of miR-1, EVI1, and calreticulin- in breast cancer and to associate their expression with clinicopathological parameters. Material & Methods: This retrospective study focused on EVI1 and calreticulin was conducted using paraffin-embedded blocks from 100 cases of breast cancer, and miR-1 gene expression analysis was performed . Results: miR-1 was downregulated in cancer patients in contrast to controls. Otherwise EVI1 & calreticulin were over-expressed. miR-1 was inversely correlated with T stage (p=0.01), lymph node metastasis (p=0.003), TNM stage (p=0.01) and ki67 (p=0.01). miR-1 was higher in the hormone-positive group. EVI1 and calreticulin were directly correlated with T stage (p=0.01 & p <0.001), lymph node metastasis (p=0.000 & p=0.01), stage (p=0.000) ki67(p=0.003), and triple-negative breast cancer (p <0.01). miR-1 was negatively correlated with both EVI1 and calreticulin (p=0.02, p= 0.000). Conclusion: miR-1, EVI1, and calreticulin might make a substantial contribution to the onset and spread of breast cancer. Therefore, upregulating miR-1 and blocking EVI1 could be possible targets for therapy in breast cancer treatment. Additionally, there might be a link between miR-1, EVI1, and calreticulin and E-cadherin in induction of epithelial–mesenchymal transition.
Source: Benha Medical Journal
Institution: Benha University
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W4413599056