Effect of Glucose Metabolism Related Protein-1 on Proliferation and Apoptosis of MIN6 Cells

Apoptosis of islet β cells participates in type 1 diabetes. Exendin-4 promotes islet β cell proliferation and inhibits apoptosis. Glucose metabolism related protein-1 (GMRP-1) has the similar effects on islet β cell. Whether the effect of exendin-4 islet β-cells is regulated by GMRP-1 is not clear. GMRP-1 siRNA or pEGFP-C3-GMRP-1 recombinant plasmid was transfected into MIN6 cells and treated with t-BHP in the presence of exendin-4 (0, 50, 100 and 200 nmol/L) followed by analysis of cell proliferation ability by CCK8 assay, apoptosis by flow cytometry, as well as GMRP-1 protein level by Western blot. After transfection of the plasmid with high expression of GMRP-1, the number of MIN6 cells was increased significantly, and the apoptosis rate was reduced (P < 0.05). With increased exendin-4 concentration, the number of cell proliferation was increased gradually with reduced cell apoptosis (P < 0.05). After the expression of GMRP-1 was decreased after GMRP-1 siRNA interference fragment transfection, the number of MIN6 cells was decreased significantly and the apoptosis was elevated (P < 0.05), whereas, exendin-4’s effect on the proliferation of MIN6 cells and inhibition of apoptosis was attenuated. GMRP-1 affects the proliferation and apoptosis of MIN6 cells, and regulates exonin-4-induced MIN6 cell proliferation and apoptosis.

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Human parathyroid hormone-related protein and human parathyroid hormone receptor type 1 are expressed in human medulloblastomas and regulate cell proliferation and apoptosis in medulloblastoma-derived cell lines

Acta Neuropathologica ◽

10.1007/s00401-007-0212-y ◽

2007 ◽

Vol 114 (2) ◽

pp. 135-145 ◽

Cited By ~ 10

Author(s):

Marco Gessi ◽

Giovanni Monego ◽

Gabriella Calviello ◽

Paola Lanza ◽

Felice Giangaspero ◽

...

Keyword(s):

Cell Proliferation ◽

Parathyroid Hormone ◽

Cell Lines ◽

Hormone Receptor ◽

Related Protein ◽

Human Parathyroid Hormone ◽

Parathyroid Hormone Receptor ◽

Parathyroid Hormone Related Protein ◽

Proliferation And Apoptosis

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Effects of miR-128 on the Proliferation and Apoptosis of Lung Cancer of Non-Small Cell by Regulating Reversion-Inducing Cysteine-Rich Protein with Kazal Motifs (RECK)

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2020.2371 ◽

2020 ◽

Vol 10 (8) ◽

pp. 1102-1108

Author(s):

Li-Qun Shan ◽

Hong-Wang Yan ◽

Hui Lin ◽

Hong-Xi Yu ◽

Bo Zhang ◽

...

Keyword(s):

Lung Cancer ◽

Cell Proliferation ◽

Small Cell ◽

Expression Level ◽

Control Group ◽

Nsclc Cell Line ◽

Related Protein ◽

Expression Levels ◽

Proliferation And Apoptosis ◽

Proliferation Ability

The study was aimed to analyse the effects of miR-128 on the proliferation and apoptosis of lung cancer cells of non-small cell by regulating RECK. The expression of miR-128 in non-small cell lung cancer (NSCLC) and its paracancerours tissues was analyzed by sequencing. miR-128 expression level in NSCLC and its paracancerours tissues was detected by qPCR. We over expressed miR-128 by mimics in A549 NSCLC cell line. Establish blank and negative control group. miR-128 and RECK expression level in each group was detected by qPCR. Use MTT assay to test the proliferation ability of each group. The apoptosis level and the level of ROS in each group were tested by hoechst 33258. The expression level of apoptosis-related protein and p38 NF- B signal pathway-related protein in each group was tested by Western blot. The results of sequencing and qPCR showed that compared with the blank control group, the expression level of miR-128 mRNA was significantly higher in the adjacent tissues than in the adjacent tissues (P < 0 05). The expression levels of miR128 mRNA and RECK mRNA in the overexpression group were significantly increased (P <0 05); the cell proliferation ability in the overexpression group was significantly reduced (P < 0 05), and the level of apoptosis was significantly increased (P < 0 05). Overexpression group Caspase-3, Bcl2/Bax, P-p38, NF-B expression levels were significantly increased (P < 0 05). MiR-128 increases ROS level in NSCLC cells, inhibits cell proliferation and promotes cell apoptosis by regulating RECK and acting on p38 NF-κB signaling pathway.

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Glucose metabolism-related protein 1 (GMRP1) regulates pancreatic beta cell proliferation and apoptosis via activation of Akt signalling pathway in rats and mice

Diabetologia ◽

10.1007/s00125-011-2048-1 ◽

2011 ◽

Vol 54 (4) ◽

pp. 852-863 ◽

Cited By ~ 14

Author(s):

X. Wang ◽

Y. Liu ◽

Z. Yang ◽

Z. Zhang ◽

W. Zhou ◽

...

Keyword(s):

Cell Proliferation ◽

Glucose Metabolism ◽

Beta Cell ◽

Pancreatic Beta Cell ◽

Signalling Pathway ◽

Beta Cell Proliferation ◽

Related Protein ◽

Proliferation And Apoptosis ◽

Rats And Mice

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Foxa2 and MafA regulate islet-specific glucose-6-phosphatase catalytic subunit-related protein gene expression

Journal of Molecular Endocrinology ◽

10.1677/jme-08-0062 ◽

2008 ◽

Vol 41 (5) ◽

pp. 315-328 ◽

Cited By ~ 10

Author(s):

Cyrus C Martin ◽

Brian P Flemming ◽

Yingda Wang ◽

James K Oeser ◽

Richard M O'Brien

Keyword(s):

Gene Expression ◽

Type 1 Diabetes ◽

Transcription Factors ◽

Binding Sites ◽

Fusion Gene ◽

Fasting Blood Glucose ◽

Catalytic Subunit ◽

Related Protein ◽

Min6 Cells

Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP/G6PC2) is a major autoantigen in both mouse and human type 1 diabetes. IGRP is selectively expressed in islet β cells and polymorphisms in the IGRP gene have recently been associated with variations in fasting blood glucose levels and cardiovascular-associated mortality in humans. Chromatin immunoprecipitation (ChIP) assays have shown that the IGRP promoter binds the islet-enriched transcription factors Pax-6 and BETA2. We show here, again using ChIP assays, that the IGRP promoter also binds the islet-enriched transcription factors MafA and Foxa2. Single binding sites for these factors were identified in the proximal IGRP promoter, mutation of which resulted in decreased IGRP fusion gene expression in βTC-3, Hamster insulinoma tumor (HIT), and Min6 cells. ChiP assays have shown that the islet-enriched transcription factor Pdx-1 also binds the IGRP promoter, but mutational analysis of four Pdx-1 binding sites in the proximal IGRP promoter revealed surprisingly little effect of Pdx-1 binding on IGRP fusion gene expression in βTC-3 cells. In contrast, in both HIT and Min6 cells mutation of these four Pdx-1 binding sites resulted in a ∼50% reduction in fusion gene expression. These data suggest that the same group of islet-enriched transcription factors, namely Pdx-1, Pax-6, MafA, BETA2, and Foxa2, directly or indirectly regulate expression of the two major autoantigens in type 1 diabetes.

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