Overcoming drug resistance in pancreatic cancer

Jiang, Long; Zhang, Yuqing; Yu, Xianjun; Yang, Jingxuan; LeBrun, Drake G.; Chen, Changyi; Yao, Qizhi; Li, Min

doi:10.1517/14728222.2011.566216

Cited by 201 publications

(183 citation statements)

References 93 publications

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“…Most patients develop resistance to gemcitabine (21), which has strong toxic side effect and is very expensive. The success of this treatment is poor and overall survival has not improved for decades (22). In recent years, much attention was paid to Chinese traditional medicine monomers (CTMM).…”

Section: Discussionmentioning

confidence: 99%

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

Liu

Zhang

et al. 2012

Oncology Reports

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Abstract. In this study, we investigated the apoptotic effect of emodin on human pancreatic cancer cell line Panc-1 in vitro and in vivo as well as the possible mechanisms involved. In vitro, human pancreatic cancer cell line Panc-1 was exposed to varying concentrations of emodin (0,10,20, 40 or 80 µmol/l). Then the mitochondrial membrane potential (MMP) was analyzed by JC-1 staining, cell apoptosis was analyzed by flow cytometry (FCM) and cell proliferation was analyzed by MTT. In vivo, nude mice orthotopically implanted were randomly divided into five groups to receive treatments by different doses of emodin: control group (normal saline 0.2 ml), E 10 group (emodin 10 mg/kg), E 20 group (emodin 20 mg/kg), E 40 group (emodin 40 mg/kg) and E 80 group (emodin 80 mg/kg). Each mouse was treated 5 times by intraperitoneal injection of emodin every 3 days. During the treatment, the feeding stuff was recorded. One week after the last treatment, we recorded the body weight and the maximum diameter of tumor in each group before the mice were sacrificed. Then the cell apoptosis of the tumor was tested by TUNEL assay. The results in vitro showed that the MMP of the cells declined and the apoptosis rate increased with the emodin concentration increasing and the cell proliferation of each group was inhibited in a dose-and time-dependent manner by emodin. The feeding stuff curve did not decline significantly in E 40 group and the apoptosis rate of the tumor cells in this group was higher than the lower-dose groups. Taken together, our results demonstrate that emodin may induce the pancreatic cancer cell apoptosis via declining the MMP and a moderate dose of emodin improved the living state of the model mice.

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Section: Discussionmentioning

confidence: 99%

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

Liu

Zhang

et al. 2012

Oncology Reports

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“…It is approved as the first line single agent treatment for advanced pancreatic cancer and for combination therapy against non-small cell lung, breast and ovarian cancers. 1 Although gemcitabine is one of the primary standard drugs used to treat various solid tumors, drug resistance often limits its efficacy, 2 making it clinically important to understand the mechanisms of gemcitabine resistance and to develop novel strategies to overcome the resistance.…”

Section: Introductionmentioning

confidence: 99%

Silencing of ribonucleotide reductase subunit M1 potentiates the antitumor activity of gemcitabine in resistant cancer cells

Wonganan

Chung

Zhu

et al. 2012

Cancer Biology & Therapy

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“…[27][28][29] However, tumor resistance of gemcitabine often seriously limits its effect. 30 These drugs may interact with DNA in two ways: by acting as structural analogs of the precursors and intermediates for the synthetic pathway, and therefore interfering with the synthesis of purines and pyrimidines, or by acting as false bases in the assembly of the DNA double helix during replication and transcription.…”

Section: Antimetabolitesmentioning

confidence: 99%

Overcoming tumor cell chemoresistance using nanoparticles: lysosomes are beneficial for (stearoyl) gemcitabine-incorporated solid lipid nanoparticles

Chen¹,

Zheng²,

Shi³

et al. 2018

IJN

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Despite recent advances in targeted therapies and immunotherapies, chemotherapy using cytotoxic agents remains an indispensable modality in cancer treatment. Recently, there has been a growing emphasis in using nanomedicine in cancer chemotherapy, and several nanomedicines have already been used clinically to treat cancers. There is evidence that formulating small molecular cancer chemotherapeutic agents into nanomedicines significantly modifies their pharmacokinetics and often improves their efficacy. Importantly, cancer cells often develop resistance to chemotherapy, and formulating anticancer drugs into nanomedicines also helps overcome chemoresistance. In this review, we briefly describe the different classes of cancer chemotherapeutic agents, their mechanisms of action and resistance, and evidence of overcoming the resistance using nanomedicines. We then emphasize on gemcitabine and our experience in discovering the unique (stearoyl) gemcitabine solid lipid nanoparticles that are effective against tumor cells resistant to gemcitabine and elucidate the underlying mechanisms. It seems that lysosomes, which are an obstacle in the delivery of many drugs, are actually beneficial for our (stearoyl) gemcitabine solid lipid nanoparticles to overcome tumor cell resistance to gemcitabine.

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Overcoming drug resistance in pancreatic cancer

Cited by 201 publications

References 93 publications

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential

Silencing of ribonucleotide reductase subunit M1 potentiates the antitumor activity of gemcitabine in resistant cancer cells

Overcoming tumor cell chemoresistance using nanoparticles: lysosomes are beneficial for (stearoyl) gemcitabine-incorporated solid lipid nanoparticles

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