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增强化疗疗效:探究紫杉醇与cd73基因抑制对乳腺癌细胞增殖和迁移的协同影响

Enhancing Chemotherapy Efficacy: Investigating the Synergistic Impact of Paclitaxel and cd73 Gene Suppression on Breast Cancer Cell Proliferation and Migration.

作者信息

Hamidnia Farzaneh, Aslan Elif S, Najafi Souzan, Baghbani Elham, Eslamkhah Sajjad, Baradaran Behzad

机构信息

Molecular Biology and Genetics, Biruni University, Istanbul, TUR.

Medical Sciences, Immunology Research Center, Tabriz University, Tabriz, IRN.

出版信息

Cureus. 2024 Jul 21;16(7):e65027. doi: 10.7759/cureus.65027. eCollection 2024 Jul.

DOI:10.7759/cureus.65027
PMID:39165432
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11334381/
Abstract

Background Enhancing chemotherapy efficacy is crucial in breast cancer treatment. This study examines the synergistic effects of paclitaxel, a common chemotherapeutic drug, and Cluster of differentiation 73 ( gene suppression via siRNA on MDA-MB-231 breast cancer cells. Methods MDA-MB-231 cells were transfected with CD73 siRNA and treated with paclitaxel. Cell viability, apoptosis, and migration were assessed by using MTT assays, Annexin V-FITC/PI staining, and wound healing assays, respectively, with flow cytometry analyzing cell cycle distribution. Results The combination of CD73 siRNA and paclitaxel significantly reduced cell viability, lowering paclitaxel's IC50 from 14.73 μg/mL to 8.471 μg/mL, indicating enhanced drug sensitivity. Apoptosis rates increased with the combination treatment, while cell migration was significantly inhibited. Flow cytometry revealed cell cycle arrest in the Sub-G1 and G2-M phases. Conclusion These findings suggest that gene suppression enhances paclitaxel's cytotoxic effects, promoting apoptosis and inhibiting cell migration in MDA-MB-231 breast cancer cell line. This combined strategy shows promise for improving breast cancer treatment outcomes by increasing the efficacy of existing chemotherapeutic regimens, warranting further research to explore its potential clinical applications and effectiveness in other breast cancer cell lines and models.

摘要

背景 提高化疗疗效在乳腺癌治疗中至关重要。本研究考察了常见化疗药物紫杉醇与通过小干扰RNA(siRNA)抑制分化簇73(CD73)基因对MDA-MB-231乳腺癌细胞的协同作用。方法 用CD73 siRNA转染MDA-MB-231细胞并给予紫杉醇处理。分别采用MTT法、膜联蛋白V-异硫氰酸荧光素/碘化丙啶(Annexin V-FITC/PI)染色和伤口愈合试验评估细胞活力、凋亡和迁移情况,并用流式细胞术分析细胞周期分布。结果 CD73 siRNA与紫杉醇联合使用显著降低了细胞活力,使紫杉醇的半数抑制浓度(IC50)从14.73 μg/mL降至8.471 μg/mL,表明药物敏感性增强。联合治疗使凋亡率增加,同时细胞迁移受到显著抑制。流式细胞术显示细胞周期停滞在亚G1期和G2-M期。结论 这些发现表明,抑制CD73基因可增强紫杉醇的细胞毒性作用,促进MDA-MB-231乳腺癌细胞系的凋亡并抑制细胞迁移。这种联合策略有望通过提高现有化疗方案的疗效来改善乳腺癌治疗效果,值得进一步研究以探索其在其他乳腺癌细胞系和模型中的潜在临床应用及有效性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/7cb34212e6d6/cureus-0016-00000065027-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/4ef501e0ba20/cureus-0016-00000065027-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/3e41bf2746fc/cureus-0016-00000065027-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/20c085e3843d/cureus-0016-00000065027-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/426a463d8947/cureus-0016-00000065027-i04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/7cb34212e6d6/cureus-0016-00000065027-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/4ef501e0ba20/cureus-0016-00000065027-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/3e41bf2746fc/cureus-0016-00000065027-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/20c085e3843d/cureus-0016-00000065027-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/426a463d8947/cureus-0016-00000065027-i04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/828f/11334381/7cb34212e6d6/cureus-0016-00000065027-i05.jpg

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