A proteomic profiling of gemcitabine resistance in pancreatic cancer cell lines

Mori-Iwamoto, Sayaka; Kuramitsu, Yasuhiro; Ryozawa, Shomei; Taba, Kumiko; Fujimoto, Masanori; Okita, Kiwamu; Nakamura, Kazuyuki; Sakaida, Isao

doi:10.3892/mmr.1.3.429

Cited by 25 publications

(26 citation statements)

References 28 publications

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“…Among them, the expression of Heat shock protein 27 (HSP27) was found to be increased in the GEMresistant cell line. Furthermore, we confirmed that GEM sensitivity was restored when the HSP27 expression in the GEM-resistant cell line was reduced (6,7). Additionally, we clarified that the expression of phosphorylated HSP27 (p-HSP27) increased in the GEM-resistant cell line (8).…”

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confidence: 63%

Heat Shock Protein 27 Expression in EUS-FNA Samples Can Predict Gemcitabine Sensitivity in Pancreatic Cancer

Kawano

Kaino

Amano

et al. 2018

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Abstract. Background/Aim: Gemcitabine (GEM) Pancreatic cancer shows one of the worst prognoses among all malignant tumors since it progresses quickly and is difficult to diagnose at an early stage. Advances in chemotherapy are considered to be important for improving the prognosis of unresectable cases.Burris et al.(1) reported that gemcitabine (GEM) can significantly prolong survival in comparison to 5-FU for unresectable pancreatic cancer. Recently, FOLFIRINOX (L-OHP, CPT-11, 5-FU, LV) therapy (2) and GEM combined with nab-paclitaxel therapy (3) were shown to prolong survival. FOLFIRINOX was associated with strong toxicity, because it has not been established whether the combination therapy can be safely administered. It is thought that GEM based-chemotherapy will also be a key to the treatment of unresectable pancreatic cancer. It has been reported that recent advances in genetic analysis technology have revealed the factors involved with GEM sensitivity in pancreatic cancer cells (4, 5), and tailored therapies are expected.We identified GEM resistance-related proteins in pancreatic cancer by a proteomic analysis. We compared the expression levels of proteins in GEM-resistant pancreatic cancer cell lines with the expression in GEM-sensitive cell lines using twodimensional electrophoresis and liquid chromatography-mass spectrometry. Among them, the expression of Heat shock protein 27 (HSP27) was found to be increased in the GEMresistant cell line. Furthermore, we confirmed that GEM sensitivity was restored when the HSP27 expression in the GEM-resistant cell line was reduced (6, 7). Additionally, we clarified that the expression of phosphorylated HSP27 (p-HSP27) increased in the GEM-resistant cell line (8).In addition, the ability to predict the treatment effects using endoscopic ultrasonography-guided fine needle aspiration (EUS-FNA) samples may help in the selection of appropriate medicines for unresectable pancreatic cancer.No previous studies have evaluated the rates of HSP27 and p-HSP27 expression in pancreatic cancer cells from EUS-FNA samples. The purpose of this study was to evaluate the rates of HSP27 and p-HSP27 expression in EUS-FNA samples, and to demonstrate their association with GEM sensitivity. Materials and Methods Subjects, Examination itemsThe comparison of the rates of HSP27 expression in the EUS-FNA samples and the resected specimens. We compared the rates of HSP27 expression in EUS-FNA samples and resected specimens and evaluated the relationship with the resected specimens. The study population included 19 patients who had been diagnosed with 637 This article is freely accessible online.Correspondence to: Michitaka Kawano,

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confidence: 63%

Heat Shock Protein 27 Expression in EUS-FNA Samples Can Predict Gemcitabine Sensitivity in Pancreatic Cancer

Kawano

Kaino

Amano

et al. 2018

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“…Many groups have reported that overexpression of HSP27 in many types of cancer is related to anti-cancer drug resistance and poor prognosis (11)(12)(13). In pancreatic cancer cells, our previous study reported that the expression level of HSP27 was elevated in gemcitabine-resistant pancreatic cancer cells compared to gemcitabine-sensitive pancreatic cancer cells (14,15). Therefore, it is thought that HSPs can be targets for anticancer drug treatment (16)(17)(18)(19).…”

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confidence: 99%

Enzyme-treated Asparagus Extract Down-regulates Heat Shock Protein 27 of Pancreatic Cancer Cells

Shimada

Nanimoto

Baron

et al. 2018

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“…The early symptoms of high-grade malignant pancreatic tumors are not clear, and thus the majority of tumors are identified at an advanced stage, yielding a low surgical resection rate (17). As a result of recent changes in human behavior and diet, the worldwide incidence of pancreatic cancer has been increasing annually (18).…”

Section: Discussionmentioning

confidence: 99%

Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling

et al. 2016

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Abstract. Paeoniflorin exhibits anticancer, anti-inflammatory and antioxidation effects, as well as specific pharmacological effects on smooth muscle and the immune, cardiovascular and central nervous systems. The present study aimed to investigate the anticancer effects of paeoniflorin on pancreatic cancer cells and to elucidate the mechanisms by which these effects occur. In the present study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assays were performed to assess cell viability and cell cytotoxicity of BXPC-3 human pancreatic cancer cells, respectively. Cellular apoptosis and caspase-3/9 activities were analyzed using an Annexin V-fluorescein isothiocyanate/propidium iodide Apoptosis Detection kit, a DAPI staining assay and colorimetric kits, respectively. Matrix metalloproteinase-9 (MMP-9) and extracellular signal-regulated kinases (ERK) protein expression in BXPC-3 cells were also investigated using gelatin zymography assays and western blot analysis, respectively. In the present study, paeoniflorin was found to inhibit the cell viability and increase cell cytotoxicity of BXPC-3 cells in a dose-and time-dependent manner. In addition, cellular apoptosis, as well as caspase-3 and -9 activity of BXPC-3 cells was increased following paeoniflorin treatment. Notably, paeoniflorin reduced MMP-9 and ERK protein expression in BXPC-3 cells. These results indicate that paeoniflorin exhibits a potential anticancer effect by enhancing human pancreatic cancer cell apoptosis via the suppression of MMP-9 and ERK signaling.

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A proteomic profiling of gemcitabine resistance in pancreatic cancer cell lines

Cited by 25 publications

References 28 publications

Heat Shock Protein 27 Expression in EUS-FNA Samples Can Predict Gemcitabine Sensitivity in Pancreatic Cancer

Heat Shock Protein 27 Expression in EUS-FNA Samples Can Predict Gemcitabine Sensitivity in Pancreatic Cancer

Enzyme-treated Asparagus Extract Down-regulates Heat Shock Protein 27 of Pancreatic Cancer Cells

Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling

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