Cytotoxicity of curcumin against CD44± prostate cancer cells: Roles of miR-383 and miR-708.

IF 1.9 Q3 CHEMISTRY, MEDICINAL Avicenna Journal of Phytomedicine Pub Date : 2023-07-01 DOI:10.22038/AJP.2023.21913
Reza Panahizadeh, Mohammad Amin Vatankhah, Farhad Jeddi, AmirAhmad Arabzadeh, Kazem Nejati-Koshki, Ramin Salimnejad, Nowruz Najafzadeh
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Abstract

Objective: Cancer stem cells (CSCs) remaining in the tumor tissues after applying treatments may cause recurrence or metastasis of prostate cancer (PC). Curcumin has the promising potential to target CSCs. Here, we aim to evaluate the cytotoxic effects of curcumin on the expression of miR-383-5p and miR-708-5p and their target genes in CD44+ CSCs and CD44- non-CSCs isolated from the PC3 prostate cancer cell line.

Materials and methods: We used MTT assay to determine the optimal cytotoxic dose of curcumin on CD44± PC cells. Then, we assessed nuclear morphological changes using DAPi staining. We used Annexin V-FITC/PI to quantify apoptotic cell death. qRT-PCR was also used to detect miRNA and gene expression levels after curcumin treatment.

Results: Curcumin significantly enhanced the apoptosis in both CD44- and CD44+ PC cells in a dose-dependent manner (p < 0.05). The cytotoxicity of curcumin against CD44- cells (IC50 40.30±2.32 μM) was found to be greater than that against CD44+ cells (IC50 83.31±2.91 μM). Also, curcumin promoted miR-383-5p and miR-708-5p overexpression while downregulating their target genes LDHA, PRDX3, and RAP1B, LSD1, respectively.

Conclusion: Our findings indicate that curcumin, by promoting the expression of tumor suppressors, miR-383-5p and miR-708-5p, and inhibiting their target genes, induced its cytotoxicity against CD44± PC cells. We trust that curcumin could be established as a promising adjuvant therapy to current PC treatment options following more research in clinical settings.

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姜黄素对CD44±前列腺癌症细胞的细胞毒性:miR-383和miR-708的作用。
目的:应用治疗后残留在肿瘤组织中的癌症干细胞(CSCs)可能导致癌症(PC)的复发或转移。姜黄素具有靶向CSC的潜力。在此,我们的目的是评估姜黄素对从PC3前列腺癌症细胞系分离的CD44+CSCs和CD44-非CSCs中miR-383-5p和miR-708-5p及其靶基因表达的细胞毒性作用。材料与方法:采用MTT法测定姜黄素对CD44±PC细胞的最佳杀伤剂量。然后,我们使用DAPi染色来评估细胞核的形态学变化。我们使用膜联蛋白V-FITC/PI来量化凋亡细胞死亡。qRT-PCR也用于检测姜黄素处理后的miRNA和基因表达水平。结果:姜黄素能显著增强CD44-和CD44+PC细胞的凋亡,且呈剂量依赖性(p<0.05),姜黄素对CD44-细胞的细胞毒作用(IC50 40.30±2.32μM)大于对CD44+细胞的细胞毒性(IC50 83.31±2.91μM)。此外,姜黄素促进miR-383-5p和miR-708-5p的过表达,同时分别下调其靶基因LDHA、PRDX3和RAP1B、LSD1。结论:姜黄素通过促进肿瘤抑制因子miR-383-5p和miR-708-5p的表达,并抑制其靶基因,诱导其对CD44±PC细胞的细胞毒性。我们相信,随着临床环境中的更多研究,姜黄素可以被确定为目前PC治疗方案的一种有前途的辅助疗法。
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来源期刊
Avicenna Journal of Phytomedicine
Avicenna Journal of Phytomedicine CHEMISTRY, MEDICINAL-
CiteScore
3.40
自引率
4.50%
发文量
17
审稿时长
6 weeks
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