miR‑200b regulates breast cancer cell proliferation and invasion by targeting radixin

Abstract

Radixin is an important member of the Ezrin-Radixin-Moesin protein family that is involved in cell invasion, metastasis and movement. microRNA (miR)-200b is a well-studied microRNA associated with the development of multiple tumors. Previous bioinformatics analysis has demonstrated that miR-200b has a complementary binding site in the 3'-untranslated region of radixin mRNA. The present study aimed to investigate the role of miR-200b in regulating radixin expression, cell proliferation and invasion in breast cancer. Breast cancer tissues at different Tumor-Node-Metastasis (TNM) stages were collected; breast tissues from patients with hyperplasia were used as a control. miR-200b and radixin mRNA expression levels were tested by reverse transcription-quantitative PCR. Radixin protein expression was detected by western blotting. The highly metastatic MDA-MB-231 cells were divided into four groups and transfected with a miR-negative control (NC), miR-200b mimic, small interfering (si)RNA-NC or siRNA targeting radixin. Cell invasion was evaluated by Transwell assay and cell proliferation was assessed by 5-ethynyl-2'-deoxyuridine staining. Compared with the control group, radixin mRNA expression was significantly higher in breast cancer tissues and increased with TNM stage. miR-200b expression levels exhibited the opposite trend. Radixin mRNA expression in breast cancer cells was notably higher, whereas miR-200b expression was lower compared with that in normal breast epithelial MCF-10A cells. The expression of radixin was higher, whereas miR-200b was lower in MDA-MB-231 cells compared with that in MCF-7 cells. miR-200b mimic or siRNA-radixin transfection downregulated the expression of radixin in MDA-MB-231 cells and attenuated the invasive and proliferative abilities of these cells. miR-200b-knockdown and radixin overexpression were associated with enhanced cell invasion in breast cancer. In conclusion, miR-200b regulates breast cancer cell proliferation and invasion by targeting radixin expression.

Re-expression of miR-200s in claudin‐low mammary tumor cells alters cell shape and reduces proliferation and invasion potentially through modulating other miRNAs and SUZ12 regulated genes

“…These studies showed that re-expression of miR-200c in MDA-MB-231 cells significantly suppressed cell migration and promoted a more rounded cell morphology [54,55], while treatment of MDA-231 cells with a miR-200c mimic was shown to significantly inhibit transwell invasion [56][57][58][59] or proliferation [57,60]. Although our current study did not find that re-expression of the miR-200b/200a/429 cluster in MDA-MB-231 cells significantly impacted proliferation or invasion, other groups have shown that treating MDA-MB-231 cells with a miR-200a mimic [61], a miR-200b mimic [62][63][64][65], a miR-429 mimic [63], or overexpressing miR-200b [66], significantly reduced migration/invasion and treating MDA-MB-231 cells with a miR-200b or miR-429 mimic significantly reduced proliferation [63,64]. It should be noted that two studies found miR-200 effects that contracted our findings.…”

Activation of GPER by E2 promotes proliferation, invasion and migration of breast cancer cells by regulating the miR‑124/CD151 pathway

“…Thus, detailed investigation of the pathogenesis of breast cancer is of considerable significance. It has been demonstrated that the prevention of metastasis is a vital factor for the effective reduction of breast cancer ( 7 , 8 ). Estrogen plays a crucial role, not only in the proliferation and initiation of breast cancer, but also in migration ( 9 ).…”

Vitamin D deficiency inhibits microRNA-196b-5p which regulates ovarian granulosa cell hormone synthesis, proliferation, and apoptosis by targeting RDX and LRRC17

“…It has been reported that RDX is a direct target of miR-196b-5p in human gastric cancer (27). Studies (28) et al (29) demonstrated that silencing the expression of RAD in pancreatic cancer cells significantly inhibited cell proliferation and tumorigenicity in vivo. RDX seems to be a positive factor in cell proliferation, but this is not reflected in our experimental results.…”