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MLLT11 siRNA 抑制 MDA-MB-231 乳腺癌细胞的迁移并促进其凋亡。

MLLT11 siRNA Inhibits the Migration and Promotes the Apoptosis of MDA-MB-231 Breast Cancer Cells.

机构信息

Shanxi Province Cancer Hospital, Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences, Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan 030001, China.

Breast Surgery, The Second Hospital of Shanxi Medical University, Taiyuan 030001, China.

出版信息

Breast J. 2023 Dec 1;2023:6282654. doi: 10.1155/2023/6282654. eCollection 2023.

DOI:10.1155/2023/6282654
PMID:38075552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10708952/
Abstract

Breast cancer is considered the most prevalent malignancy due to its high incidence rate, recurrence, and metastasis in women that makes it one of the deadliest cancers. The current study aimed to predict the genes associated with the recurrence and metastasis of breast cancer and to validate their effect on MDA-MB-231 cells. Through the bioinformatics analysis, the transcription factor 7 cofactor (MLLT11) as the target gene was obtained. MLLT11-specific siRNA was synthesized and transfected into MDA-MB-231 cells. The results demonstrated that the siRNA significantly reduced the MLLT11 mRNA levels. Moreover, cell migration and invasion, as well as the protein levels of phosphatidylinositol 3-kinase (PI3K), AKT, matrix metalloproteinase (MMP) 2, and MMP9, were significantly lower in the groups treated with siRNA while the apoptosis was augmented. Collectively, MLLT11 siRNA elicited ameliorative properties on breast cancer cells, possibly via the inhibition of the PI3K/AKT signaling pathway.

摘要

乳腺癌被认为是最常见的恶性肿瘤,因为其在女性中的发病率、复发率和转移率高,使其成为最致命的癌症之一。本研究旨在预测与乳腺癌复发和转移相关的基因,并验证其对 MDA-MB-231 细胞的影响。通过生物信息学分析,获得了转录因子 7 辅助因子(MLLT11)作为靶基因。合成了 MLLT11 特异性 siRNA 并转染至 MDA-MB-231 细胞。结果表明,siRNA 显著降低了 MLLT11 mRNA 水平。此外,用 siRNA 处理的细胞迁移和侵袭以及磷酸肌醇 3-激酶(PI3K)、AKT、基质金属蛋白酶(MMP)2 和 MMP9 的蛋白水平显著降低,而细胞凋亡增加。总之,MLLT11 siRNA 对乳腺癌细胞具有改善作用,可能是通过抑制 PI3K/AKT 信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/ad627df6e131/TBJ2023-6282654.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/2aaac0cd2253/TBJ2023-6282654.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/e0b167965201/TBJ2023-6282654.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/4d8efa104be0/TBJ2023-6282654.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/ad627df6e131/TBJ2023-6282654.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/2aaac0cd2253/TBJ2023-6282654.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/4a4c5686daef/TBJ2023-6282654.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/cbec0e7ed47b/TBJ2023-6282654.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/e0b167965201/TBJ2023-6282654.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/4d8efa104be0/TBJ2023-6282654.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ec9/10708952/ad627df6e131/TBJ2023-6282654.007.jpg

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