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去甲斑蝥素通过诱导内质网应激抑制宫颈癌的恶性进展。

Norcantharidin inhibits the malignant progression of cervical cancer by inducing endoplasmic reticulum stress.

机构信息

Department of Gynecology, Tongliao City Hospital, Tongliao, Inner Mongolia Autonomous Region, P.R. China.

出版信息

Mol Med Rep. 2024 May;29(5). doi: 10.3892/mmr.2024.13195. Epub 2024 Mar 8.

DOI:10.3892/mmr.2024.13195
PMID:38456480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10955518/
Abstract

The antitumor effect of norcantharidin (NCTD) has been widely reported. However, whether NCTD can inhibit cervical cancer remains unknown. In the present study, it was shown that NCTD inhibited the viability of cervical cancer cells and caused cell cycle arrest in a concentration‑dependent manner. Further analysis revealed that the NCTD‑induced reduction in cell viability could be reversed by the inhibitor of apoptosis z‑VAD‑FMK and by the inhibitor of endoplasmic reticulum (ER) stress, 4‑phenylbutyric acid (4‑PBA). Additionally, NCTD led to the accumulation of reactive oxygen species as well as a decrease in the mitochondrial membrane potential in cervical cancer cells, whereas 4‑PBA pre‑treatment attenuated these alterations. In addition, NCTD increased the expression of the apoptosis‑related proteins Bip, activating transcription factor (ATF) 4 and C/EBP homologous protein in a concentration‑dependent manner. Moreover, NCTD significantly increased the expression of the ER stress‑related signaling molecules protein kinase R‑like ER kinase, inositol‑requiring enzyme 1 and ATF6, but 4‑PBA abolished these effects. experiments showed that NCTD significantly inhibited the growth of subcutaneous tumors in mice. Additionally, the expression of ER stress‑related molecules and apoptosis‑related proteins increased significantly after NCTD treatment. In conclusion, NCTD induces apoptosis by activating ER stress and ultimately curtails the progression of cervical cancer.

摘要

去甲斑蝥素（NCTD）的抗肿瘤作用已被广泛报道。然而，NCTD 是否能抑制宫颈癌尚不清楚。在本研究中，结果表明 NCTD 以浓度依赖的方式抑制宫颈癌细胞的活力并导致细胞周期停滞。进一步分析表明，凋亡抑制剂 z-VAD-FMK 和内质网（ER）应激抑制剂 4-苯丁酸（4-PBA）可逆转 NCTD 诱导的细胞活力降低。此外，NCTD 导致宫颈癌细胞中活性氧的积累和线粒体膜电位的降低，而 4-PBA 预处理可减弱这些变化。此外，NCTD 以浓度依赖的方式增加凋亡相关蛋白 Bip、激活转录因子（ATF）4 和 C/EBP 同源蛋白的表达。此外，NCTD 显著增加了 ER 应激相关信号分子蛋白激酶 R 样 ER 激酶、肌醇需求酶 1 和 ATF6 的表达，但 4-PBA 消除了这些作用。实验表明，NCTD 可显著抑制小鼠皮下肿瘤的生长。此外，NCTD 处理后 ER 应激相关分子和凋亡相关蛋白的表达显著增加。综上所述，NCTD 通过激活 ER 应激诱导细胞凋亡，从而抑制宫颈癌的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/d20e359f2262/mmr-29-05-13195-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/c87c0d53a262/mmr-29-05-13195-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/29465c22fbea/mmr-29-05-13195-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/33e2d42e50d0/mmr-29-05-13195-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/848281b7bfe9/mmr-29-05-13195-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/73d04085acaa/mmr-29-05-13195-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/936bac1e9903/mmr-29-05-13195-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/d20e359f2262/mmr-29-05-13195-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/c87c0d53a262/mmr-29-05-13195-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/29465c22fbea/mmr-29-05-13195-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/33e2d42e50d0/mmr-29-05-13195-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/848281b7bfe9/mmr-29-05-13195-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/73d04085acaa/mmr-29-05-13195-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/936bac1e9903/mmr-29-05-13195-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8749/10955518/d20e359f2262/mmr-29-05-13195-g06.jpg

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