Overexpression of mir-183 and mir-494 promotes proliferation and migration in human breast cancer cell lines.
نویسندگان
چکیده
Breast cancer (BC) is a leading cause of cancer-associated mortality in females worldwide. MicroRNAs (miRNAs or miRs), a type of non-coding RNA, have been reported to be important in the regulation of BC onset and progression. Several studies have implicated the role of miR-183 and miR-494 in different types of cancer. However, the biological functions of these miRNAs in BC remain largely unknown. In the present study, the expression of both miRNAs was assessed in the MDA-MB-231 and MDA-MB-468 BC cell lines. It was hypothesized that miR-183 and miR-494 serve an important role in regulating the expression of key genes associated with the metastatic phenotype of BC cells. To further understand their role, the expression of these miRNAs was restored in selected BC cell lines. Functional assays revealed that overexpression of miR-183 or miR-494 modulated the proliferation and migration of MDA-MB-231 and MDA-MB-468 cells in vitro. Additionally, retinoblastoma 1 (RB1) was identified to be a downstream target of both miRNAs by in silico analysis. Western blotting revealed that upregulation of miR-183 was associated with downregulation of RB1 protein in MDA-MB-231 cells. In conclusion, the present results support the hypothesis that miR-183 and miR-494 serve a pivotal role in BC metastasis, and that miR-183 may act as an oncogene by targeting RB1 protein in MDA-MB-231 cells.
منابع مشابه
MiR-6165 Dysregulation in Breast Cancer and Its Effect on Cell Proliferation and Migration
Background: ncRNAs have been identified as oncogenic drivers and tumor suppressors in any type of cancer. Although many classes of ncRNAs have been reported, most studies have been performed on microRNAs (miRNAs). miRNAs can regulate several target genes and affect important processes such as homeostasis, angiogenesis, cell proliferation, differentiation, and apoptosis. Located in the p75NTR ge...
متن کاملmiR-92a promotes hepatocellular carcinoma cells proliferation and invasion by FOXA2 targeting
Objective(s): MicroRNAs (miRNAs) are considered as powerful, post-transcriptional regulators of gene expression in hepatocellular carcinoma cells (HCC). However, the function of miR-92a is still unclear in HCC. Materials and Methods: Expression of miR-92a in human HCC cell lines was evaluated using qRT-PCR. MTT assay and transwell assay were used to examine the function of miR-92a in HepG2 and ...
متن کاملThe miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer
Objective(s): To explore the correlation between expression patterns and functions of miR-383 and LDHA in hepatocellular cancer (HCC). Materials and Methods: We detected the expression of miR-383 and LDHA in 30 HCC tissues and their matched adjacent normal tissues using qRT-PCR. Then we performed MTT assay, foci formation assay, transwell migration assay, glucose uptake assay and lactate produc...
متن کاملEvaluation of miR-34a Effect on CCND1 mRNA Level and Sensitization of Breast Cancer Cell Lines to Paclitaxel
Background: A growing body of literature has revealed the effective role of miR-34a, as a tumor suppressor and regulator of expression of multiple targets in tumorigenesis and cancer progression. This study aimed at evaluating the potential effects of miR-34a alone or in combination with paclitaxel on breast cancer cells. Methods: After miR-34a transduction by lentiviral vectors in two MCF-7 an...
متن کاملmiR‑494 is an independent prognostic factor and promotes cell migration and invasion in colorectal cancer by directly targeting PTEN.
Accumulating evidence has shown that micro-RNAs (miRNAs) are involved in multiple processes in cancer development and progression. Upregulation of miRNA-494 (miR-494) has been identified as an oncogenic miRNA and is associated with poor prognosis in several types of human cancer. However, the specific function of miR-494 in colorectal cancer remains unclear. In this study we found that the expr...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Oncology letters
دوره 14 1 شماره
صفحات -
تاریخ انتشار 2017