Tannic acid elicits differential gene regulation in prostate cancer apoptosis.

IF 2.1 4区医学 Q3 PHARMACOLOGY & PHARMACY Acta Pharmaceutica Pub Date : 2024-09-14 Print Date: 2024-09-01 DOI:10.2478/acph-2024-0020

Sinan Kandir, Sevtap Karakurt, Çiğdem Gökçek-Saraç, Serdar Karakurt

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Abstract

Prostate cancer is a significant global health concern that requires innovative therapeutic investigations. Here, the potential anticancer properties of tannic acid were evaluated by examining its effects on apoptosis in prostate cancer cell lines. PC-3 and LnCaP prostate adeno carcinoma cells, along with PNT1A prostate control cells, were cultured and divided into untreated and tannic acid-treated groups. Cell proliferation, cytotoxicity, and effects of tannic acid on the cell death mechanism were evaluated. mRNA expression levels of 84 genes were explored in cells following tannic acid treatment. Notably, tannic acid-induced down-regulation of several pro-survival genes, including ATM, BCL2, BCL2A1, BIK, BIRC2, BIRC3, BRE, CASP3, CASP6, CASP8, CHEK2, CRADD, PPIA, RPA3, TNFSF18, TRAF1, TRAF2, TRAF4, and TRAF5 in both cell lines. Moreover, tannic acid treatment led to the up-regulation of various pro-apoptotic genes, such as BCL10, BIRC3, BNIP3, CASP1, CASP5, CD40, CIDEB, DAPK2, FASLG, GADD45A, MYD88, RPA 3, TNFRSF10D, TNFRSF17, TNFRSF8, TNFSF13B, TNFSF4, TNFSF7, TNFSF8, TNFSF9, TP53, TRAF1, and TRAF2 in both PC-3 and LnCap cells. These findings highlight tannic acid's ability to induce apoptosis in prostate cancer cells through pro-apoptotic pathways. This study concludes that tannic acid selectively inhibits prostate cancer cell growth.

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单宁酸在前列腺癌凋亡过程中引发不同的基因调控。

前列腺癌是全球关注的重大健康问题，需要创新的治疗研究。在此，我们通过研究单宁酸对前列腺癌细胞系凋亡的影响来评估其潜在的抗癌特性。培养 PC-3 和 LnCaP 前列腺腺癌细胞以及 PNT1A 前列腺对照细胞，并将其分为未处理组和单宁酸处理组。对单宁酸处理后细胞中 84 个基因的 mRNA 表达水平进行了研究。值得注意的是，单宁酸在两种细胞系中都诱导了一些促生存基因的下调，包括 ATM、BCL2、BCL2A1、BIK、BIRC2、BIRC3、BRE、CASP3、CASP6、CASP8、CHEK2、CRADD、PPIA、RPA3、TNFSF18、TRAF1、TRAF2、TRAF4 和 TRAF5。此外，单宁酸处理还导致了多种促凋亡基因的上调，如 BCL10、BIRC3、BNIP3、CASP1、CASP5、CD40、CIDEB、DAPK2、FASLG、GADDK2、CRADD、PPIA、RPA3、TNFSF18、TRAF1、TRAF2、TRAF4 和 TRAF5、PC-3 和 LnCap 细胞中的 FASLG、GADD45A、MYD88、RPA 3、TNFRSF10D、TNFRSF17、TNFRSF8、TNFSF13B、TNFSF4、TNFSF7、TNFSF8、TNFSF9、TP53、TRAF1 和 TRAF2。这些发现突显了单宁酸通过促凋亡途径诱导前列腺癌细胞凋亡的能力。本研究得出结论，单宁酸可选择性地抑制前列腺癌细胞的生长。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Acta Pharmaceutica PHARMACOLOGY & PHARMACY-

CiteScore

5.20

自引率

3.60%

发文量

审稿时长

>12 weeks

期刊介绍： AP is an international, multidisciplinary journal devoted to pharmaceutical and allied sciences and contains articles predominantly on core biomedical and health subjects. The aim of AP is to increase the impact of pharmaceutical research in academia, industry and laboratories. With strong emphasis on quality and originality, AP publishes reports from the discovery of a drug up to clinical practice. Topics covered are: analytics, biochemistry, biopharmaceutics, biotechnology, cell biology, cell cultures, clinical pharmacy, drug design, drug delivery, drug disposition, drug stability, gene technology, medicine (including diagnostics and therapy), medicinal chemistry, metabolism, molecular modeling, pharmacology (clinical and animal), peptide and protein chemistry, pharmacognosy, pharmacoepidemiology, pharmacoeconomics, pharmacodynamics and pharmacokinetics, protein design, radiopharmaceuticals, and toxicology.