As a common female malignancy, triple-negative breast cancer (TNBC) is the most serious subtype in breast cancer (BC). BAALC binder of MAP3K1 and KLF4 (BAALC) is a common oncogene in acute myelocytic leukemia (AML). We sought to explore the role of BAALC in TNBC. In this study, BAALC was significantly upregulated in TNBC tissues and cells. Then, the results of functional assays disclosed that BAALC facilitated cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) processes, but repressed cell apoptosis in TNBC. Next, miR-380-3p was identified as the upstream of BAALC in TNBC cells. Moreover, LRRC75A-AS1 (also named small nucleolar RNA host gene 29: SNHG29) was verified to act as the sponge of miR-380-3p to elevate BAALC expression in TNBC. Besides, LRRC75A-AS1 could negatively regulate miR-380-3p but positively regulate BAALC expression. Finally, rescue assays elucidated that LRRC75A-AS1 facilitated cell proliferation, invasion, and EMT processes in TNBC by targeting miR-380-3p/BAALC pathway. Taken together, our study revealed a novel ceRNA network of LRRC75A-AS1/miR-380-3p/ BAALC in accelerating TNBC development, indicating new promising targets for TNBC treatment.
Long noncoding RNA (lncRNA) MAF BZIP transcription factor G antisense RNA 1 (MAFG-AS1) has been demonstrated to serve an important role in the progression of various types of cancer, whereas its role in breast cancer has not been fully elucidated. The present study aimed to explore the potential role and underlying mechanism of MAFG-AS1 in breast cancer. To achieve this, the expression of MAFG-AS1, microRNA (miR)-150-5p and MYB was detected by reverse transcription-quantitative PCR. The binding between miR-150-5p and MAFG-AS1 or MYB was verified using a luciferase reporter assay. Cell proliferation was analyzed by MTS, apoptosis and cell cycle were detected by Annexin V/propidium iodide, and cell migration was analyzed by wound healing assay. The results demonstrated that the expression levels of MAFG-AS1 were significantly upregulated in breast cancer tissues and cells compared with those in normal breast tissues and cells. High MAFG-AS1 expression promoted the proliferation, migration and epithelial-mesenchymal transition of breast cancer cells. By contrast, miR-150-5p expression was reduced in breast cancer tissues compared with that in healthy breast tissues, and low expression of miR-150-5p was associated with poor overall survival in patients with breast cancer. Bioinformatics and luciferase assay revealed that MAFG-AS1 served as a sponge of miR-150-5p, and that miR-150-5p bound to MYB. The functional rescue assay results demonstrated that MAFG-AS1 knockdown suppressed the proliferation and migration of breast cancer cells by regulating miR-150-5p, which in turn targeted MYB. In conclusion, the results of the present study demonstrated that MAFG-AS1 functioned as a novel oncogenic lncRNA in the development of human breast cancer via regulating the miR-150-5p/MYB axis, which suggested that MAFG-AS1 may be a novel biomarker for the diagnosis and prognosis of human breast cancer.
Breast cancer displays high morbidity and mortality. despite exerting certain effects, traditional treatments cannot eliminate every cancer cell and may kill normal cells due to inaccurate targeting. However, as a traditional chinese medicine, capsaicin, an active compound extracted from chili peppers, has displayed potent anticarcinogenic activities in vitro and in vivo, but the underlying mechanism is not completely understood. The pharmacological effects of capsaicin on tumors was evaluated in Mda MB 231 breast cancer cells. The MTT, cell scratch assay, cell cycle analysis, cell transfection, reverse transcription-quantitative Pcr and western blotting were performed to investigate the potential antitumor mechanisms of capsaicin. in the present study, the potential anticancer mechanism underlying capsaicin in Mda-MB-231 cells in vitro was investigated. capsaicin significantly inhibited Mda-MB-231 breast cancer cell viability and migration compared with the control group. The flow cytometry results indicated that capsaicin induced G 2 /M cell cycle arrest in Mda-MB-231 cells. in addition, capsaicin significantly reduced the expression of cyclin-dependent kinase 8 (cdK8) in breast cancer cells compared with the control group. Moreover, lV-cdK8 small interfering rna-transduced Mda-MB-231 cells displayed lower cdK8 mrna and protein expression levels compared with lV-negative control-shrna-transduced cells. Furthermore, capsaicin significantly reduced the expression levels of phosphorylated (p)-Pi3K, p-akt, Wnt and β-catenin in vitro compared with the control group. collectively, the results of the present study suggested that capsaicin inhibited breast cancer cell viability, induced G 2 /M cell cycle arrest, reduced cdK8 expression levels, decreased the phosphorylation of Pi3K and akt and downregulated Wnt and β-catenin expression levels in Mda-MB-231 cells.
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