Gold Nanoparticles sensitize pancreatic cancer cells to gemcitabine.

IF 4.1 Q2 CELL BIOLOGY Cell Stress Pub Date : 2019-07-31 DOI:10.15698/cst2019.08.195

Yanyan Huai, Yushan Zhang, Xunhao Xiong, Shamik Das, Resham Bhattacharya, Priyabrata Mukherjee

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Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest solid cancers with dismal prognosis. Several mechanisms that are mainly responsible for aggressiveness and therapy resistance of PDAC cells include epithelial to mesenchymal transition (EMT), stemness and Mitogen Activated Protein Kinase (MAPK) signaling. Strategies that inhibit these mechanisms are critically important to improve therapeutic outcome in PDAC. In the current study, we wanted to investigate whether gold nanoparticles (AuNPs) could sensitize pancreatic cancer cells to the chemotherapeutic agent gemcitabine. We demonstrated that treatment with AuNPs of 20 nm diameter inhibited migration and colony forming ability of pancreatic cancer cells. Pre-treatment with AuNPs sensitized pancreatic cancer cells to gemcitabine in both viability and colony forming assays. Mechanistically, pre-treatment of pancreatic cancer cells with AuNPs decreased gemcitabine induced EMT, stemness and MAPK activation. Taken together, these findings suggest that AuNPs could be considered as a potential agent to sensitize pancreatic cancer cells to gemcitabine.

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金纳米粒子使癌症胰腺细胞对吉西他滨敏感。

胰腺导管腺癌（PDAC）是最致命的实体癌之一，预后极差。主要导致PDAC细胞侵袭性和治疗耐药性的几种机制包括上皮-间充质转化（EMT）、干性和丝裂原活化蛋白激酶（MAPK）信号传导。抑制这些机制的策略对于改善PDAC的治疗效果至关重要。在目前的研究中，我们想研究金纳米颗粒（AuNP）是否可以使胰腺癌症细胞对化疗剂吉西他滨敏感。我们证明用直径为20nm的AuNPs处理抑制了胰腺癌症细胞的迁移和集落形成能力。在生存力和集落形成测定中，AuNP预处理使癌症胰腺细胞对吉西他滨敏感。从机制上讲，用AuNP预处理胰腺癌症细胞降低了吉西他滨诱导的EMT、干性和MAPK活化。总之，这些发现表明AuNPs可以被认为是一种潜在的使胰腺癌症细胞对吉西他滨敏感的药剂。

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

Cell Stress Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (miscellaneous)

CiteScore

13.50

自引率

0.00%

发文量

审稿时长

15 weeks

期刊介绍： Cell Stress is an open-access, peer-reviewed journal that is dedicated to publishing highly relevant research in the field of cellular pathology. The journal focuses on advancing our understanding of the molecular, mechanistic, phenotypic, and other critical aspects that underpin cellular dysfunction and disease. It specifically aims to foster cell biology research that is applicable to a range of significant human diseases, including neurodegenerative disorders, myopathies, mitochondriopathies, infectious diseases, cancer, and pathological aging. The scope of Cell Stress is broad, welcoming submissions that represent a spectrum of research from fundamental to translational and clinical studies. The journal is a valuable resource for scientists, educators, and policymakers worldwide, as well as for any individual with an interest in cellular pathology. It serves as a platform for the dissemination of research findings that are instrumental in the investigation, classification, diagnosis, and therapeutic management of major diseases. By being open-access, Cell Stress ensures that its content is freely available to a global audience, thereby promoting international scientific collaboration and accelerating the exchange of knowledge within the research community.