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miR-383与顺铂对肺癌细胞生长、增殖及迁移抑制的协同作用

Synergistic Effect of miR-383 and Cisplatin on Inhibition of Growth, Proliferation, and Migration of Lung Cancer Cells.

作者信息

Elyaszadeh Vagef, Tohidast Maryam, Hosseini Seyed Samad, Amini Mohammad, Marami Parinaz, Baradaran Behzad, Mokhtarzadeh Amir Ali, Jebelli Asiyeh

机构信息

Department of Biological Science, Faculty of Basic Science, Higher Education Institute of Rab-Rashid, Tabriz, Iran.

Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

Arch Iran Med. 2025 May 1;28(5):264-274. doi: 10.34172/aim.33450.

Abstract

BACKGROUND

Lung cancer (LC) is a common life-threatening malignancy in humans. Cisplatin has been widely used in the treatment of various types of cancer. miR-383 is dysregulated in multiple cancers, and participates in tumorigenic processes, including apoptosis, proliferation, metastasis, and drug resistance. This study aimed to investigate the synergistic effect of miR-383 and cisplatin in LC.

METHODS

A549 cells were treated with cisplatin and miR-383 separately or in combination. Cell viability, apoptosis induction, stemness features, migratory capacity, and autophagy were measured by various methods. In addition, quantitative real-time PCR (qRT-PCR) was used to evaluate the expression levels of genes involved in apoptosis, stemness, and migration.

RESULTS

The results demonstrated that miR-383 transfection in A549 cells increased their chemosensitivity to cisplatin, enhancing cisplatin-induced apoptosis (from 11.28% to 37.86%). This effect was mediated by regulating key genes such as and (<0.0001). Moreover, the combination of miR-383 and cisplatin synergistically reduced cell migration and colony formation. It also downregulated metastatic and stemness-related genes, including and , respectively (<0.0001).

CONCLUSION

The findings indicate that the combination treatment of miR-383 and cisplatin suppressed cell proliferation, migration and colony formation while enhancing the sensitivity of A549 cells to chemotherapy compared to monotherapy. These results suggest that miR-383 combination therapy warrants further investigation as a potential strategy for LC treatment.

摘要

背景

肺癌(LC)是人类常见的危及生命的恶性肿瘤。顺铂已广泛应用于各种类型癌症的治疗。miR-383在多种癌症中表达失调,并参与肿瘤发生过程,包括细胞凋亡、增殖、转移和耐药性。本研究旨在探讨miR-383与顺铂在肺癌中的协同作用。

方法

分别或联合用顺铂和miR-383处理A549细胞。通过各种方法检测细胞活力、诱导凋亡、干性特征、迁移能力和自噬。此外,采用定量实时PCR(qRT-PCR)评估参与细胞凋亡、干性和迁移的基因表达水平。

结果

结果表明,在A549细胞中转染miR-383可增加其对顺铂的化疗敏感性,增强顺铂诱导的细胞凋亡(从11.28%增至37.86%)。这种作用是通过调控关键基因如 和 介导的(<0.0001)。此外,miR-383与顺铂联合使用可协同减少细胞迁移和集落形成。它还分别下调了与转移和干性相关的基因,包括 和 (<0.0001)。

结论

研究结果表明,与单一疗法相比,miR-383与顺铂联合治疗可抑制细胞增殖、迁移和集落形成,同时增强A549细胞对化疗的敏感性。这些结果表明,miR-383联合疗法作为肺癌治疗的潜在策略值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/240c/12305408/39f00aa0f8f6/aim-28-264-g004.jpg

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