Sodium Butyrate as Histone Deacetylase Inhibitor Can Alter miR-101, ZEB1, ZEB2, and E-cadherin Expression in MDA-MB-468 Cells as Triple Negative Breast Cancer Cells

IF 0.4 Q4 ONCOLOGY

International Journal of Cancer Management Pub Date : 2024-01-07 DOI:10.5812/ijcm-139329

Sama Layegh Ahani, A. Niknejad, Elaheh Amini

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Abstract

Background: Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype in women worldwide. The various alterations in the expression of different microRNAs (miRNAs) have been reported as crucial in the development of metastasis in breast tumors. Objectives: This study investigated the effect of sodium butyrate (NaB) on cell survival, cell metastasis and expression of miR-101, ZEB1, ZEB2 and E- cadherin in MDA-MB-468 cells as a TNBC cell line. Methods: Cell viability was evaluated using the (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT assay), and the metastasis potential of MDA-MB-468 cells was investigated using the scratch and transwell assay. The expression of genes involved in the metastasis process was measured using real-time polymerase chain reaction (PCR). Results: The MTT assay showed that NaB attenuated MDA-MB-468 cell survival dose-dependently with an IC50 value of 3.1 mM after 72 h treatment. The scratch and transwell assays also showed the anti-metastatic potential of NaB. The expression of miR-101, E-cadherin, ZEB1, and ZEB2 was significantly difference in MDA-MB-468 cells treated with 3.1 mM NaB after 72 hours (P < 0.05). E-cadherin and miR-101 were up-regulated, while the expression of ZEB1 and ZEB2 was significantly down-regulated compared to the untreated cells. This suggests that NaB increased cell attachment and prevented metastasis. In addition, NaB (IC50 value) restored the expression of miR-101, as a tumor suppressor, in MDA-MB-468 cells confirming its anti-cancer potency. Conclusions: Sodium butyrate can be used as a drug to suppress invasion and cell migration in TNBC cells. However, further studies are needed to demonstrate the putative anti-metastatic mechanism of NaB in preclinical and clinical settings.

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作为组蛋白去乙酰化酶抑制剂的丁酸钠可改变三阴性乳腺癌细胞 MDA-MB-468 中的 miR-101、ZEB1、ZEB2 和 E-cadherin 表达

背景：三阴性乳腺癌（TNBC三阴性乳腺癌（TNBC）是全球女性中最具侵袭性的乳腺癌亚型。据报道，不同微 RNA（miRNA）表达的各种改变对乳腺肿瘤的转移发展至关重要。研究目的本研究探讨了丁酸钠（NaB）对 TNBC 细胞系 MDA-MB-468 细胞的细胞存活、细胞转移以及 miR-101、ZEB1、ZEB2 和 E-粘连蛋白表达的影响。研究方法用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四氮唑（MTT 法）评估细胞活力，用划痕法和经孔法研究 MDA-MB-468 细胞的转移潜力。利用实时聚合酶链反应（PCR）测定了转移过程中相关基因的表达。结果显示MTT 试验表明，NaB 可剂量依赖性地降低 MDA-MB-468 细胞的存活率，处理 72 小时后的 IC50 值为 3.1 mM。划痕试验和透孔试验也显示了 NaB 的抗转移潜力。经 3.1 mM NaB 处理的 MDA-MB-468 细胞在 72 小时后，miR-101、E-cadherin、ZEB1 和 ZEB2 的表达均有显著差异（P < 0.05）。与未处理的细胞相比，E-cadherin 和 miR-101 表达上调，而 ZEB1 和 ZEB2 表达明显下调。这表明 NaB 增加了细胞的附着力并阻止了转移。此外，NaB（IC50 值）还能恢复 MDA-MB-468 细胞中作为肿瘤抑制因子的 miR-101 的表达，这证实了它的抗癌功效。结论丁酸钠可作为一种药物抑制 TNBC 细胞的侵袭和细胞迁移。然而，还需要进一步的研究来证明 NaB 在临床前和临床环境中的抗转移机制。

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来源期刊

International Journal of Cancer Management ONCOLOGY-

CiteScore

1.10

自引率

0.00%

发文量

期刊介绍： International Journal of Cancer Management (IJCM) publishes peer-reviewed original studies and reviews on cancer etiology, epidemiology and risk factors, novel approach to cancer management including prevention, diagnosis, surgery, radiotherapy, medical oncology, and issues regarding cancer survivorship and palliative care. The scope spans the spectrum of cancer research from the laboratory to the clinic, with special emphasis on translational cancer research that bridge the laboratory and clinic. We also consider original case reports that expand clinical cancer knowledge and convey important best practice messages.