miR-638 represses the stem cell characteristics of breast cancer cells by targeting E2F2
| Autor: | Jia-Qi Wang, Qiu-Yan Lin, Pei-Rui Chen, Li-Li Wu, Wei-E Zheng |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Mice Nude Breast Neoplasms Flow cytometry law.invention Mice 03 medical and health sciences 0302 clinical medicine Breast cancer E2F2 Transcription Factor SOX2 law medicine Animals Humans Pharmacology (medical) Radiology Nuclear Medicine and imaging Cell Self Renewal RNA Small Interfering E2F Transcription factor Cell Proliferation E2F2 Binding Sites medicine.diagnostic_test business.industry General Medicine medicine.disease Gene Expression Regulation Neoplastic MicroRNAs Hyaluronan Receptors 030104 developmental biology Oncology 030220 oncology & carcinogenesis MCF-7 Cells Neoplastic Stem Cells Cancer research Suppressor Female Stem cell business Neoplasm Transplantation |
| Zdroj: | Breast Cancer. 27:147-158 |
| ISSN: | 1880-4233 1340-6868 |
| Popis: | The miR-638 acted as a tumor suppressor and E2F transcription factor 2 (E2F2) was a critical regulator in some cancers, while the role of them on stemness of breast cancer stem cells (BCSCs) was rarely detailed. Hence, we focused on exploring the effects of miR-638 and E2F2 on BCSCs stemness. The proportion of CD24 −/CD44 + cells of BCSCs was detected by flow cytometry. The target relationship of miR-638 and E2F2 was explored using luciferase assays. The ability of self-renewal, proliferation, and invasion of BCSCs were determined by Mammosphere forming, Cell Counting Kit-8 (CCK-8), colony formation, and transwell assays. Xenograft tumor was established to detect the influence of miR-638 on tumor growth. miR-638 was down-regulated, while E2F2 was elevated in breast cancer. The E2F2 level was negatively correlated with miR-638. The BCSCs represented higher proportion of CD24 −/CD44 + cells and levels of sex determining region Y-box 2 (SOX2) and octamer-binding transcription factor 4 (OCT4). The miR-638 was down-regulated and E2F2 was increased in BCSCs. MiR-638 could target to E2F2 and decreased the level of E2F2 in BCSCs cells. Overexpression of miR-638 decreased the proportion of CD24 −/CD44 + cells and the levels of SOX2 and OCT4 by inhibiting E2F2. The overexpression of miR-638 also inhibited the abilities of self-renewal, proliferation, and invasion of BCSCs by inhibiting E2F2. The miR-638 overexpression inhibited the breast tumor growth. MiR-638 represses the characteristics and behaviors of BCSCs by targeting E2F2. MiR-638 may be a potential target for breast cancer therapy. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink