Identification of Differentiation-Related Proteins in Gastric Adenocarcinoma Tissues by Proteomics

Zhou, Xin; Yao, Kun; Zhang, Lang; Zhang, Ying; Han, Yin; Liu, Huiling; Liu, Xiangwen; Su, Gang; Yuan, Wenzhen; Wei, Xinlei; Guan, Quan-Lin; Zhu, Bin

doi:10.1177/1533034615595792

Cited by 9 publications

(12 citation statements)

References 31 publications

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“…Tu et al 17 demonstrated in vitro that decreasing the expression of the ENO1 gene through small interfering RNA in tamoxifen-resistant breast cancer cells significantly enhanced 4-hydroxytamoxifen-induced cytotoxicity. Zhou et al 8 showed that the ENO1 expression was closely correlated with the tumor differentiation. The expression of ENO1 in 55 cases of gastric carcinoma tissues and 23 cases of gastric ulcer tissue was detected by Ni et al , 18 and this study revealed that the expression of ENO1 in gastric cancer tissues was significantly higher than that in gastric ulcer tissues ( P < .01) and positively related to differentiation grade, depth of invasion, lymph node metastasis, and TNM staging ( P < .05).…”

Section: Discussionmentioning

confidence: 99%

“…We speculated that gastric cancer cells also have an altered metabolism, and using proteomics and immunohistochemistry, we found that the expression of α-enolase (ENO1), a key enzyme in glycolysis, was increased in the early stages of cancer. 8 In this study, we constructed a eukaryotic expression vector encoding a short hairpin RNA (shRNA) that specifically targeted ENO1 and downregulated its expression in the gastric cancer MKN45 cell line. Determining the effects of ENO1 on gastric cancer cell growth and proliferation and on cell sensitivity to chemotherapeutic drugs may provide a new theoretical basis for gastric cancer gene treatment.…”

Section: Introductionmentioning

confidence: 99%

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Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells

Qiao

Wang

et al. 2018

Technol Cancer Res Treat

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α-Enolase is a significant subunit of enolase and acts as a glycolytic enzyme responsible for catalyzing the conversion of 2-phosphoglycerate to phosphoenolpyruvate in the anaerobic glycolysis pathway. The research about their role is known little in tumor invasion and metastasis. This research analyzed the effect of α-enolase in proliferation and progression of human gastric cancer. The constructed PLKO.1-ENO1 shRNA vector was transfected into 293 T cells and used to infect gastric cancer cells, MKN45, by using lentivirus method. Negative controls were generated by infection with viruses containing empty vector PLKO.1-scramble-shRNA by the same protocol and using wild-type MKN45 cells as blank control. The silencing effect was confirmed by reverse transcription polymerase chain reaction and Western blotting at messenger RNA and protein levels, respectively. Cell proliferation and chemosensitivity were tested by methyl-thiazolyl-tetrazolium assay. Cell apoptosis was tested by flow cytometry. The cell line α-enolase short hairpin RNA stabling silence α-enolase was successfully constructed. In the α-enolase short hairpin RNA cell lines, messenger RNA and protein expression of α-enolase were significantly lower than those in negative control and blank control groups. The proliferation and clone formation ability were significantly inhibited, cell apoptosis was increased significantly, and the inhibition rate of chemotherapy drugs was increased (P < .05). Our data provide strong evidence that α-enolase short hairpin RNA interference vector can effectively suppress the proliferation and increase chemosensitivity of MKN45 cells, which may provide a novel gene therapy for gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells

Qiao

Wang

et al. 2018

Technol Cancer Res Treat

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“…The Warburg effect has been hypothesised to be an adaptation mechanism in cancer cells to support the biosynthetic requirements of rapid proliferation. Alpha-enolase expression has been shown to be altered at the mRNA and/or protein level in a range of tumours [ Table 1], and generally upregulated in most, including acute myeloid leukaemia (AML), glioma, melanoma, lymphoma, and colorectal, endometrial, gastric, head and neck, liver, ovarian and pancreatic cancer [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] .…”

Section: Alpha-enolase Expression Is Altered In Tumours and Varies Wimentioning

confidence: 99%

“…Increased glycolysis is considered a hallmark of cancer [2] and investigating glycolytic enzymes may yield new therapeutic approaches for cancer treatment. Enolases are key glycolytic enzymes [3] , and increased expression of one isoform, a-enolase, has been identified in several cancer types [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] . This review provides an overview of the expression of a-enolase and key functions it controls in cancer cells, with a focus on the potential role of a-enolase as a cancer prognostic biomarker or therapeutic target.…”

Section: Introductionmentioning

confidence: 99%

Unlikely role of glycolytic enzyme ��-enolase in cancer metastasis and its potential as a prognostic biomarker

Schofield¹,

Lincz²,

Skelding³

2020

JCMT

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Reliance on glycolysis for energy production is considered a hallmark of cancer and the glycolytic enzyme a-enolase is overexpressed in a range of cancer types. However, recent studies have revealed that a-enolase is involved in a variety of unrelated physiological processes and can be found in multiple unexpected cellular locations. This review focuses on the unlikely role of a-enolase as an extracellular plasminogen-binding receptor localised to the plasma membrane. Conversion of plasminogen to plasmin on the surface of cancer cells enhances their ability to invade through stroma by activating collagenases and degrading fibrin as well as extracellular matrix proteins. Increased expression of a-enolase is associated with increased migration and invasion of cancer cells, and decreased metastasis-free survival in patients with several cancer types, including non-small cell lung, pancreatic, breast and colorectal cancers. Due to its overexpression in a range of cancer types and multi-functional roles in key areas of tumour metabolism and metastasis, a-enolase may be useful as a universal cancer prognostic biomarker or therapeutic target.

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“…The expression of CRT in tumor tissues such as liver, stomach and colon cancers is higher than in normal tissues [ 22 ] as well as in urinary system tumors. CRT has been proposed as a potential biomarker for bladder cancer [ 14 , 23 , 24 ]. In our previous study, CRT level was found higher in patients with drug-sensitive EC and lower in patients with drug-resistant EC.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress-mediated membrane expression of CRT/ERp57 induces immunogenic apoptosis in drug-resistant endometrial cancer cells

Chen

et al. 2017

Oncotarget

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ObjectiveTo investigate the role of endoplasmic reticulum (ER) stress-mediated CRT/ERp57 complex expression underlying the mechanism of resistance to doxorubicin (DOX) in endometrial carcinoma (EC) in vivo and in vitro.MethodsThe expression of CRT, ERp57, p-PERK, eIF2α, p-eIF2α in EC patients and EC cells was detected by Western blots and by immunofluorescence assay. MTT assay was used to determine the LC50 of EC cells to DOX and cell viability. Apoptosis was assayed using flow cytometer. The protein expression of PERK, cleaved-caspase-8, p-eIF2α and CHOP were detected by Western blot, and the expression of VAMP-1, SNAP23 and PERK was knockdown by siRNA and/or shRNA. The expression of CRT/ERp57 complex was detected by flow cytometry. In addition, the expression of eIF2α and p-eIF2α was detected by Western blot analysis after drug-resistant EC cells were transfected with lentivirus overexpressing CRT, treated with GADD34 inhibitor and ES stress inducer. MTT assay was used to detect the phagocytic activity of T cells induced by maturation of dendritic cells in drug-resistant EC cells.ResultsThe expression of CRT, ERp57, p-PERK and p-eIF2α was significantly decreased in the drug-resistant patients in EC patients. The IC50 of the drug-resistant EC cells was 10 times higher than that of the wild type cells. In the drug-resistant EC cells the expression of CRT, ERp57, p-PERK, p-eIF2α, caspase-8 and CHOP was significantly lower than in the wild type cells. After treatment with DOX, CRT and ER stress-related proteins p-PERK, p-eIF2α, caspase-8 and apoptosis were significantly increased in wild-type EC cells, but not in drug-resistant EC cells. The increased expressions led to inhibition of cell growth and apoptosis. The knockdown of PERK gene and addition of DOX resulted in significant decrease of cleaved-caspase 8 and p-eIF2α in sensitive EC cells. The expression of CRT/ERp57 in sensitive EC cells was further significantly decreased by blocking VAMP and SNAP23. In addition, transfection with CRT overexpressing lentivirus and addition of GADD34 inhibitor and ER stress inducer in drug-resistant EC cells revealed a significant increase in the expression of CRT/ERp57 complex and p-eIF2α when DOX was added simultaneously, which promoted the maturation and chemotaxis of T lymphocytes to phagocytose drug-resistant EC cells.ConclusionDOX can induce the death of tumor cells by ER stress-mediated CRT/ERp57 expression in EC cells. Induction of ER stress in drug-resistant EC cells up-regulates the membrane expression of CRT/ERp57, enhances phagocytosis, induces immunogenic apoptosisand sensitizes the cells to DOX.

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Identification of Differentiation-Related Proteins in Gastric Adenocarcinoma Tissues by Proteomics

Cited by 9 publications

References 31 publications

Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells

Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells

Unlikely role of glycolytic enzyme ��-enolase in cancer metastasis and its potential as a prognostic biomarker

Endoplasmic reticulum stress-mediated membrane expression of CRT/ERp57 induces immunogenic apoptosis in drug-resistant endometrial cancer cells

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