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哈尔明抑制胰腺癌细胞的增殖，并使胰腺癌对吉西他滨治疗敏感。

Harmine suppresses the proliferation of pancreatic cancer cells and sensitizes pancreatic cancer to gemcitabine treatment.

作者信息

Wu Lin-Wen, Zhang Jian-Kang, Rao Mingjun, Zhang Zuo-Yan, Zhu Hua-Jian, Zhang Chong

机构信息

School of Medicine, Zhejiang University City College, Hangzhou, Zhejiang 310015, People's Republic of China.

College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, People's Republic of China.

出版信息

Onco Targets Ther. 2019 Jun 12;12:4585-4593. doi: 10.2147/OTT.S205097. eCollection 2019.

DOI:10.2147/OTT.S205097
PMID:31354292
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6580126/
Abstract

PURPOSE

Pancreatic carcinoma is one of the most deadliest types of cancer, and relatively insensitive to the currently available chemotherapy. Thus, the discovery of novel therapeutic agents to prolong the survival times of patients with pancreatic cancer is urgently required.

METHODS

Cell proliferation was assessed using the sulforhodamine B and cell clone formation assay, apoptosis was analyzed through Annexin V/PI staining, analysis of cell cycle distribution was determined by PI staining, and the expression of proteins was detected via Western blotting.

RESULTS

Our data showed that harmine exerted an anti-proliferative effect and cell cycle arrest at G2/M in pancreatic cancer cells. Meanwhile, harmine plus gemcitabine showed strong synergy in inhibiting the proliferation of pancreatic cancer cells. Furthermore, harmine induced apoptosis and enhanced the gemcitabine-induced apoptosis in pancreatic cancer cells. The AKT/mTOR pathway is involved in mechanisms of gemcitabine resistance in pancreatic cancer cells, our data demonstrated that harmine plus gemcitabine significantly suppressed the AKT/mTOR signaling pathway.

CONCLUSION

Harmine may be a potential candidate for the treatment of pancreatic cancer. Morever, the combination of harmine with gemcitabine appears to be an attractive option for the treatment of patients with pancreatic cancer.

摘要

目的

胰腺癌是最致命的癌症类型之一，对目前可用的化疗相对不敏感。因此，迫切需要发现新的治疗药物来延长胰腺癌患者的生存时间。

方法

使用磺基罗丹明B和细胞克隆形成试验评估细胞增殖，通过膜联蛋白V/碘化丙啶染色分析细胞凋亡，通过碘化丙啶染色确定细胞周期分布分析，并通过蛋白质印迹检测蛋白质表达。

结果

我们的数据表明，骆驼蓬碱在胰腺癌细胞中发挥抗增殖作用并使细胞周期停滞在G2/M期。同时，骆驼蓬碱加吉西他滨在抑制胰腺癌细胞增殖方面显示出强大的协同作用。此外，骆驼蓬碱诱导胰腺癌细胞凋亡并增强吉西他滨诱导的凋亡。AKT/mTOR信号通路参与胰腺癌细胞对吉西他滨耐药的机制，我们的数据表明，骆驼蓬碱加吉西他滨显著抑制AKT/mTOR信号通路。

结论

骆驼蓬碱可能是治疗胰腺癌的潜在候选药物。此外，骆驼蓬碱与吉西他滨联合使用似乎是治疗胰腺癌患者的一个有吸引力的选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/4510cedb461b/OTT-12-4585-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/e27da5b7dddc/OTT-12-4585-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/2f2b2675f08c/OTT-12-4585-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/a49e17c94304/OTT-12-4585-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/4510cedb461b/OTT-12-4585-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/e27da5b7dddc/OTT-12-4585-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/2f2b2675f08c/OTT-12-4585-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/a49e17c94304/OTT-12-4585-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5924/6580126/4510cedb461b/OTT-12-4585-g0004.jpg

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