SIPL1, Regulated by MAZ, Promotes Tumor Progression and Predicts Poor Survival in Human Triple-Negative Breast Cancer

Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer owing to a lack of effective targeted therapy and acquired chemoresistance. Here, we explored the function and mechanism of shank-interacting protein-like 1 (SIPL1) in TNBC progression. SIPL1 expression was examined in hu...

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Bibliographic Details
Published in:Frontiers in oncology 2021-12, Vol.11, p.766790-766790
Main Authors: He, Juanjuan, Wang, Jing, Li, Teng, Chen, Kunlun, Li, Songchao, Zhang, Shaojin
Format: Article
Language:English
Subjects:
Akt
MAZ
NF-κB
Oncology
SIPL1
triple-negative breast cancer
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Summary:Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer owing to a lack of effective targeted therapy and acquired chemoresistance. Here, we explored the function and mechanism of shank-interacting protein-like 1 (SIPL1) in TNBC progression. SIPL1 expression was examined in human TNBC tissues and cell lines by quantitative reverse transcription PCR, western blot, and immunohistochemistry. overexpression and silenced cell lines were established in BT-549 and MDA-MB-231 cells. The biological functions of SIPL1 in TNBC were studied using the CCK-8 assay, CellTiter-Glo Luminescent Cell Viability assay, caspase-3/8/9 assay, wound healing assay, and transwell assay and using a nude mouse model. The potential mechanisms underlying the effects of SIPL1 on TNBC progression were explored using bioinformatics analysis, luciferase reporter assays, and chromatin immunoprecipitation followed by qPCR. expression was higher in human TNBC tissues and cell lines than in adjacent normal tissues and a breast epithelial cell line (MCF10A). High expression of was positively correlated with poor overall and disease-free survival in patients with TNBC. overexpression elevated and silencing repressed the malignant phenotypes of TNBC cells . overexpression promoted xenograft tumor growth . Myc-associated zinc-finger protein (MAZ) transcriptionally activated . Finally, we found that SIPL1 promoted TNBC malignant phenotypes activation of the AKT/NF-κB signaling pathways. These results indicate that the MAZ/SIPL1/AKT/NF-κB axis plays a crucial role in promoting the malignant phenotypes of TNBC cells.
ISSN:2234-943X
2234-943X
DOI:10.3389/fonc.2021.766790