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том 82 издание 5 страницы 829-838

A novel TRAIL mutant-TRAIL-Mu3 enhances the antitumor effects by the increased affinity and the up-expression of DR5 in pancreatic cancer

Тип публикацииJournal Article
Дата публикации2018-08-24
scimago Q1
wos Q3
БС1
SJR0.969
CiteScore5.7
Impact factor2.3
ISSN03445704, 14320843
Cancer Research
Oncology
Pharmacology
Pharmacology (medical)
Toxicology
Краткое описание
Pancreatic cancer is a malignant tumor of the digestive system with poor prognosis and high mortality, and the treatment of pancreatic cancer still remains a major challenge. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis selectively in cancer cells while causing virtually no damage to normal cells, which is promising for cancer therapy. However, many primary tumors and cancer cell lines including various human pancreatic cancer cell lines were found to be resistant to TRAIL-induced apoptosis. Therefore, the purpose of the study was to improve antitumor effect of TRAIL on pancreatic cancer. The 114–121 amino acid coding sequence “VRERGPQR” of wild type TRAIL protein that was selected changed into “RRRRRRRR”, and the novel membrane-penetrating peptide-alike mutant protein was named TRAIL-Mu3. The antitumor effect of TRAIL-Mu3 was analyzed both in vitro and in vivo. Western blotting, immunofluorescence and flow cytometry were used to investigate the underlying mechanisms. TRAIL-Mu3 could enhance the antitumor effects on pancreatic cancer cell lines, and the antitumor effect of TRAIL-Mu3 was stronger than gemcitabine in vivo. The immunofluorescence results suggested that TRAIL-Mu3 could remarkably enhance the affinity to pancreatic cancer cells. The Western blot results showed that treatment with TRAIL-Mu3 caused a clear cleavage of caspase-3 and caspase-8. In addition, both the Western blot and flow cytometry suggested a significantly up-expression of DR5 in TRAIL-Mu3 group. Membrane-penetrating peptide-alike mutant-TRAIL-Mu3 induced pancreatic cancer cell death more efficiently than TRAIL, and this effect was supposed to be mediated by the increased affinity to cell membrane, the up-regulation of DR5 and the enhancement of activated caspase.
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Huang M. et al. A novel TRAIL mutant-TRAIL-Mu3 enhances the antitumor effects by the increased affinity and the up-expression of DR5 in pancreatic cancer // Cancer Chemotherapy and Pharmacology. 2018. Vol. 82. No. 5. pp. 829-838.
ГОСТ со всеми авторами (до 50) Скопировать
Huang M., Zhu H., Yi C., Juan Y., Wei L., Yang X., Chen S., Huang Y. A novel TRAIL mutant-TRAIL-Mu3 enhances the antitumor effects by the increased affinity and the up-expression of DR5 in pancreatic cancer // Cancer Chemotherapy and Pharmacology. 2018. Vol. 82. No. 5. pp. 829-838.
RIS |
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TY - JOUR
DO - 10.1007/s00280-018-3658-9
UR - https://doi.org/10.1007/s00280-018-3658-9
TI - A novel TRAIL mutant-TRAIL-Mu3 enhances the antitumor effects by the increased affinity and the up-expression of DR5 in pancreatic cancer
T2 - Cancer Chemotherapy and Pharmacology
AU - Huang, Min
AU - Zhu, Hong
AU - Yi, Cheng
AU - Juan, Yan
AU - Wei, Lijia
AU - Yang, Xi
AU - Chen, Shouchun
AU - Huang, Ying
PY - 2018
DA - 2018/08/24
PB - Springer Nature
SP - 829-838
IS - 5
VL - 82
PMID - 30167846
SN - 0344-5704
SN - 1432-0843
ER -
BibTex |
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@article{2018_Huang,
author = {Min Huang and Hong Zhu and Cheng Yi and Yan Juan and Lijia Wei and Xi Yang and Shouchun Chen and Ying Huang},
title = {A novel TRAIL mutant-TRAIL-Mu3 enhances the antitumor effects by the increased affinity and the up-expression of DR5 in pancreatic cancer},
journal = {Cancer Chemotherapy and Pharmacology},
year = {2018},
volume = {82},
publisher = {Springer Nature},
month = {aug},
url = {https://doi.org/10.1007/s00280-018-3658-9},
number = {5},
pages = {829--838},
doi = {10.1007/s00280-018-3658-9}
}
MLA
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Huang, Min, et al. “A novel TRAIL mutant-TRAIL-Mu3 enhances the antitumor effects by the increased affinity and the up-expression of DR5 in pancreatic cancer.” Cancer Chemotherapy and Pharmacology, vol. 82, no. 5, Aug. 2018, pp. 829-838. https://doi.org/10.1007/s00280-018-3658-9.