Abstract
The aberrant expression of miRNA is strongly linked to numerous stages of triple-negative breast cancer (TNBC) progression, and it plays an indispensable role in the process from tumor onset and progress to invasion and metastasis. In this study, we first transfected miR-129-1-3p mimics and inhibitor into MDA-MB-231 TNBC cells, respectively. Then, we assessed the pathological role of miR-129-1-3p in MDA-MB-231 cells. The results showed that miR-129-1-3p were successfully inserted into MDA-MB-231 cells. Besides, miR-129-1-3p could distinctively repress the growth, migration along with infiltration of MDA-MB-231 cells, which might be related to the inhibition of GRIN2D expression. Our results indicate that miR-129-1-3p was illustrated to serve as a tumor repressor via targeting GRIN2D in TNBC cells and highlight that the restoration of miR-129-1-3p might be a new treatment target for TNBC.
Highlights
triple-negative breast cancer (TNBC) is an aggressive subclass of breast cancer (BC), representing around 10–20% of all invasive BCs [1, 2]
We detected the expression of Matrix metallopeptidase 9 (MMP-9), CD147, Matrix metallopeptidase 2 (MMP-2), as well as VEGF protein linked to tumor cell migration along with infiltration in MDA-MB-231 cells via Western blot experiment
The results showed that miR-129-1-3p mimics reduced the expression of CD147, MMP-2, MMP-9, and VEGF protein in MDA-MB-231 cells, whereas miR129-1-3p inhibitor had the opposite influence (Figure 5)
Summary
TNBC (triple-negative breast cancer) is an aggressive subclass of breast cancer (BC), representing around 10–20% of all invasive BCs [1, 2]. As TNBC does not respond to endocrine treatment and always shows low effectiveness to targeted therapy, chemotherapy is still the most effective method of preventing cancer cell growth along with metastasis [3]. Investigations have documented that miRNAs may play diverse roles in different kinds of cancers, with some acting as tumor repressor genes and others as oncogenes, depending on the pathway or gene they modulate [12–14]. It is known that miR-129-1-3p can interfere with tumor occurrence and prognosis through acting on diverse molecular targets in serous ovarian cancer, gastric cancer, as well as non-small cell lung cancer [16–18]. We purposed to study the mediating role of miRNA-129-1-3p in repressing the growth, migration, as well as infiltration of TNBC cells to supply evidence for the development of new medication for the disease
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