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抗生素替加环素通过下调胰腺导管腺癌中的 CCNE2 抑制细胞增殖、迁移和侵袭。

Antibiotic tigecycline inhibits cell proliferation, migration and invasion via down-regulating CCNE2 in pancreatic ductal adenocarcinoma.

机构信息

State Key Laboratory of Silkworm Genome Biology, Institute of Sericulture and Systems Biology, Southwest University, Beibei, Chongqing, China.

Cancer Center, Medical Research Institute, Southwest University, Beibei, Chongqing, China.

出版信息

J Cell Mol Med. 2020 Apr;24(7):4245-4260. doi: 10.1111/jcmm.15086. Epub 2020 Mar 6.

DOI:10.1111/jcmm.15086
PMID:32141702
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7171345/
Abstract

Recently, many researches have reported that antibiotic tigecycline has significant effect on cancer treatment. However, biomedical functions and molecular mechanisms of tigecycline in human pancreatic ductal adenocarcinoma (PDAC) remain unclear. In the current study, we tried to assess the effect of tigecycline in PDAC cells. AsPC-1 and HPAC cells were treated with indicated concentrations of tigecycline for indicated time, and then, MTT, BrdU and soft agar assay were used to test cell proliferation. The effect of tigecycline on cell cycle and cellular apoptosis was tested by cytometry. Migration and invasion were detected by wound healing assay and transwell migration/invasion assay. Expressions of cell cycle-related and migration/invasion-related protein were determined by using Western blot. The results revealed that tigecycline observably suppressed cell proliferation by inducing cell cycle arrest at G0/G1 phase and blocked cell migration/invasion via holding back the epithelial-mesenchymal transition (EMT) process in PDAC. In addition, tigecycline also remarkably blocked tumorigenecity in vivo. Furthermore, the effects of tigecycline alone or combined with gemcitabine in vitro or on PDAC xenografts were also performed. The results showed that tigecycline enhanced the chemosensitivity of PDAC cells to gemcitabine. Interestingly, we found CCNE2 expression was declined distinctly after tigecycline treatment. Then, CCNE2 was overexpressed to rescue tigecycline-induced effect. The results showed that CCNE2 overexpression significantly rescued tigecycline-inhibited cell proliferation and migration/invasion. Collectively, we showed that tigecycline inhibits cell proliferation, migration and invasion via down-regulating CCNE2, and tigecycline might be used as a potential drug for PDAC treatment alone or combined with gemcitabine.

摘要

最近，许多研究报告称抗生素替加环素对癌症治疗有显著效果。然而，替加环素在人胰腺导管腺癌（PDAC）中的生物医学功能和分子机制仍不清楚。在本研究中，我们试图评估替加环素在 PDAC 细胞中的作用。用不同浓度的替加环素处理 AsPC-1 和 HPAC 细胞不同时间，然后用 MTT、BrdU 和软琼脂实验检测细胞增殖。用流式细胞术检测替加环素对细胞周期和细胞凋亡的影响。用划痕愈合实验和 Transwell 迁移/侵袭实验检测迁移和侵袭。用 Western blot 检测细胞周期相关和迁移/侵袭相关蛋白的表达。结果表明，替加环素通过诱导 G0/G1 期细胞周期停滞明显抑制细胞增殖，并通过抑制上皮-间充质转化（EMT）过程阻断 PDAC 细胞迁移/侵袭。此外，替加环素还显著抑制体内肿瘤发生。此外，还在体外或 PDAC 异种移植物中进行了替加环素单独或与吉西他滨联合的效果研究。结果表明，替加环素增强了 PDAC 细胞对吉西他滨的化疗敏感性。有趣的是，我们发现替加环素处理后 CCNE2 的表达明显下降。然后，过表达 CCNE2 以挽救替加环素诱导的作用。结果表明，CCNE2 的过表达显著挽救了替加环素抑制的细胞增殖和迁移/侵袭。总之，我们表明替加环素通过下调 CCNE2 抑制细胞增殖、迁移和侵袭，替加环素可能单独或与吉西他滨联合用于 PDAC 的治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/11345959dc3a/JCMM-24-4245-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/573eb1ea27c9/JCMM-24-4245-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/dd2290738bf7/JCMM-24-4245-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/652a4a5b6c63/JCMM-24-4245-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/577de388d60a/JCMM-24-4245-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/6b17dff217a9/JCMM-24-4245-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/09186fff448a/JCMM-24-4245-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/ef19897e28a4/JCMM-24-4245-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/11345959dc3a/JCMM-24-4245-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/573eb1ea27c9/JCMM-24-4245-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/dd2290738bf7/JCMM-24-4245-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/652a4a5b6c63/JCMM-24-4245-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/577de388d60a/JCMM-24-4245-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/6b17dff217a9/JCMM-24-4245-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/09186fff448a/JCMM-24-4245-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/ef19897e28a4/JCMM-24-4245-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8e7/7171345/11345959dc3a/JCMM-24-4245-g008.jpg

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Tigecycline as a dual inhibitor of retinoblastoma and angiogenesis via inducing mitochondrial dysfunctions and oxidative damage.替加环素通过诱导线粒体功能障碍和氧化损伤，作为视网膜母细胞瘤和血管生成的双重抑制剂。
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