Background Dysregulation of microRNAs (miRNAs) was found to play crucial roles in varieties of cancers, which affect tumor proliferation and migration. MiR-27a-3p has been identified as a tumor-related miRNA in liver cancer, lung cancer, and colorectal cancer. However, the function of miR-27a-3p in triple-negative breast cancer (TNBC) and its possible molecular mechanisms have still not been elucidated. Methods QRT-PCR technique was used to detect the expression of miR-27a-3p in TNBC and normal breast cell lines or the effects of miR-27a-3p knockdown and overexpression in TNBC cell lines. Proliferation and migration were measured by CCK-8 method, colony formation, wound healing, and Transwell assays, respectively. Furthermore, we used a dual-luciferase reporter gene assay and Western blot analysis to identify GSK3β as a target of miR-27a-3p. Results In this study, we found that miR-27a-3p expression was significantly elevated in TNBC cell lines. Database analysis suggested that TNBC patients with a high expression of miR-27a-3p have poorer overall survival possibilities. Overexpression of miR-27a-3p promotes TNBC cells proliferation, colony formation, and cell migration in vitro. Nevertheless, dual-luciferase reporter result showed that miR-27a-3p directly targeted the 3ʹ-UTR regions of GSK3β mRNA and negatively regulated its expression. Lastly, we demonstrated that miR-27a-3p inactivates Wnt/β-catenin signaling pathway via targeting GSK3β. Conclusion These results indicate that expression of miR-27a-3p was highly expressed in TNBC and promoted tumor progression through attenuating GSK3β and may have a potential molecular-targeted strategy for TNBC therapy.

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Introduction: Intracranial branch atheromatous disease (BAD) has been applied to occlusions that occur at the origin of large caliber penetrating arteries due to the microatheromas or large parent artery plaques. This study aimed to explore the association between culprit plaques of large parent arteries, neuroimaging markers of cerebral small vessel disease (CSVD), and the risk of early neurological deterioration (END) in stroke patients with BAD. Methods: A total of 97 stroke patients with BAD in the vascular territories of the lenticulostriate arteries or paramedian pontine arteries, diagnosed using high-resolution magnetic resonance imaging (HRMRI), were prospectively recruited in this observational study. A culprit plaque in the middle cerebral artery was defined as the only arterial plaque on the ipsilateral side of an infarction visible on diffusion-weighted imaging. A culprit plaque in the basilar artery (BA) was identified when it was observed within the same axial slices of an infarction or on the adjacent upper or lower slice, whereas a plaque within the BA located in the ventral region was considered non-culprit. If more than one plaque was present in the same vascular territory, the most stenotic plaque was chosen for the analysis. Four CSVD neuroimaging markers, including white matter hyperintensity (WMH), lacunes, microbleeds, and enlarged perivascular spaces (EPVS), were evaluated in accordance with the total CSVD score. The associations between neuroimaging features of lesions within large parent arteries, neuroimaging markers of CSVD, and the risk of END in stroke patients with BAD were investigated using logistic regression analysis. Results: END occurred in 41 stroke patients (42.27%) with BAD. The degree of large parent artery stenosis (P<0.001), culprit plaques of large parent arteries (P<0.001), and plaque burden (P<0.001) were significantly different between the END and non-END groups in stroke patients with BAD. In logistic regression analysis, culprit plaques of large parent arteries (OR, 32.258; 95% CI, 4.140-251.346) were independently associated with the risk of END in stroke patients with BAD. Conclusions: Culprit plaques of large parent arteries could predict the risk of END in stroke patients with BAD. These results suggest that lesions in the large parent arteries, rather than damage to the cerebral small vessels, contribute to END in stroke patients with BAD.

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