Insulin gene enhancer protein 1 mediates glycolysis and tumorigenesis of gastric cancer through regulating glucose transporter 4

Insulin gene enhancer protein 1, (ISL1), a LIM‐homeodomain transcription factor, is involved in multiple tumors and is associated with insulin secretion and metabolic phenotypes. However, the role of ISL1 in stimulating glycolysis to promote tumorigenesis in gastric cancer (GC) is unclear. In this study, we aimed to characterize the expression pattern of ISL1 in GC patients and explore its molecular biological mechanism in glycolysis and tumorigenesis.

[1]  A. Ricci,et al.  Expression and role of p16 and GLUT1 in malignant diseases and lung cancer: A review , 2020, Thoracic cancer.

[2]  Q. Ding,et al.  METTL3-mediated m6A modification of HDGF mRNA promotes gastric cancer progression and has prognostic significance , 2019, Gut.

[3]  Jinlong Wang,et al.  Prognostic roles of MAGE family members in breast cancer based on KM-Plotter Data , 2019, Oncology letters.

[4]  Fei Liu,et al.  Apatinib inhibits glycolysis by suppressing the VEGFR2/AKT1/SOX5/GLUT4 signaling pathway in ovarian cancer cells , 2019, Cellular Oncology.

[5]  D. Gibson,et al.  Selective androgen receptor modulators (SARMs) have specific impacts on the mouse uterus , 2019, The Journal of endocrinology.

[6]  Xiaoping Zhou,et al.  KLF8 is associated with poor prognosis and regulates glycolysis by targeting GLUT4 in gastric cancer , 2019, Journal of cellular and molecular medicine.

[7]  S. Bhattacharya,et al.  Pioneering function of Isl1 in the epigenetic control of cardiomyocyte cell fate , 2019, Cell Research.

[8]  M. Chikri,et al.  DNAJB3 attenuates metabolic stress and promotes glucose uptake by eliciting Glut4 translocation , 2019, Scientific Reports.

[9]  J. Ji,et al.  ISL1 predicts poor outcomes for patients with gastric cancer and drives tumor progression through binding to the ZEB1 promoter together with SETD7 , 2019, Cell Death & Disease.

[10]  E. Radford.  Exploring the extent and scope of epigenetic inheritance , 2018, Nature Reviews Endocrinology.

[11]  Cheng Li,et al.  GEPIA: a web server for cancer and normal gene expression profiling and interactive analyses , 2017, Nucleic Acids Res..

[12]  Minoru Kanehisa,et al.  KEGG: new perspectives on genomes, pathways, diseases and drugs , 2016, Nucleic Acids Res..

[13]  N. Hay,et al.  Reprogramming glucose metabolism in cancer: can it be exploited for cancer therapy? , 2016, Nature Reviews Cancer.

[14]  N. Waterhouse,et al.  Analyzing Cell Death by Nuclear Staining with Hoechst 33342. , 2016, Cold Spring Harbor protocols.

[15]  Ping Chen,et al.  PDX1 and ISL1 differentially coordinate with epigenetic modifications to regulate insulin gene expression in varied glucose concentrations , 2016, Molecular and Cellular Endocrinology.

[16]  D. Reinberg,et al.  ISL1 and JMJD3 synergistically control cardiac differentiation of embryonic stem cells , 2016, Nucleic acids research.

[17]  J. Locasale,et al.  The Warburg Effect: How Does it Benefit Cancer Cells? , 2016, Trends in biochemical sciences.

[18]  A. Jemal,et al.  Cancer statistics in China, 2015 , 2016, CA: a cancer journal for clinicians.

[19]  Ping Chen,et al.  ISL-1 promotes pancreatic islet cell proliferation by forming an ISL-1/Set7/9/PDX-1 complex , 2015, Cell cycle.

[20]  P. Hruz,et al.  In Silico Modeling-based Identification of Glucose Transporter 4 (GLUT4)-selective Inhibitors for Cancer Therapy* , 2015, The Journal of Biological Chemistry.

[21]  Johannes Zuber,et al.  Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis , 2015, Nature Communications.

[22]  Ping Chen,et al.  ISL-1 is overexpressed in non-Hodgkin lymphoma and promotes lymphoma cell proliferation by forming a p-STAT3/p-c-Jun/ISL-1 complex , 2014, Molecular Cancer.

[23]  M. Stolte,et al.  Development of gastric cancer and its prevention. , 2014, Archives of Iranian medicine.

[24]  G. Semenza,et al.  HIF-1 mediates metabolic responses to intratumoral hypoxia and oncogenic mutations. , 2013, The Journal of clinical investigation.

[25]  M. Vieth,et al.  ISL1 expression is not restricted to pancreatic well-differentiated neuroendocrine neoplasms, but is also commonly found in well and poorly differentiated neuroendocrine neoplasms of extrapancreatic origin , 2013, Modern Pathology.

[26]  M. Tan,et al.  Targeting cellular metabolism to improve cancer therapeutics , 2013, Cell Death and Disease.

[27]  David E. Muench,et al.  c-Myc and Cancer Metabolism , 2012, Clinical Cancer Research.

[28]  Ping Chen,et al.  ISL1 Promotes Pancreatic Islet Cell Proliferation , 2011, PloS one.

[29]  P. Sutphin,et al.  Targeting GLUT1 and the Warburg Effect in Renal Cell Carcinoma by Chemical Synthetic Lethality , 2011, Science Translational Medicine.

[30]  Yunfu Sun,et al.  Isl1 Is required for multiple aspects of motor neuron development , 2011, Molecular and Cellular Neuroscience.

[31]  M. Rigoulet,et al.  The Warburg and Crabtree effects: On the origin of cancer cell energy metabolism and of yeast glucose repression. , 2011, Biochimica et biophysica acta.

[32]  Ping Chen,et al.  POU homeodomain protein OCT1 modulates islet 1 expression during cardiac differentiation of P19CL6 cells , 2011, Cellular and Molecular Life Sciences.

[33]  Tianshu Liu,et al.  Lentiviral-mediated siRNA targeted against osteopontin suppresses the growth and metastasis of gastric cancer cells. , 2011, Oncology reports.

[34]  D. Hanahan,et al.  Hallmarks of Cancer: The Next Generation , 2011, Cell.

[35]  Angélica Figueroa,et al.  Potential Role of Sugar Transporters in Cancer and Their Relationship with Anticancer Therapy , 2010, International journal of endocrinology.

[36]  Y. Mok,et al.  Surgical outcomes and prognostic factors for T4 gastric cancers. , 2009, Asian journal of surgery.

[37]  Ping Chen,et al.  The LIM-homeodomain protein ISL1 activates insulin gene promoter directly through synergy with BETA2. , 2009, Journal of molecular biology.

[38]  K. Kinzler,et al.  Glucose Deprivation Contributes to the Development of KRAS Pathway Mutations in Tumor Cells , 2009, Science.

[39]  R. Stein,et al.  Islet-1 is Required for the Maturation, Proliferation, and Survival of the Endocrine Pancreas , 2009, Diabetes.

[40]  H. Moch,et al.  Islet 1 (Isl1) Expression is a Reliable Marker for Pancreatic Endocrine Tumors and Their Metastases , 2008, The American journal of surgical pathology.

[41]  Jill P. Mesirov,et al.  GSEA-P: a desktop application for Gene Set Enrichment Analysis , 2007, Bioinform..

[42]  J. Best,et al.  Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer , 2005, Journal of cellular physiology.

[43]  R. Gillies,et al.  Why do cancers have high aerobic glycolysis? , 2004, Nature Reviews Cancer.

[44]  M. Armoni,et al.  The Tumor Suppressor p53 Down-Regulates Glucose Transporters GLUT1 and GLUT4 Gene Expression , 2004, Cancer Research.

[45]  A. Becker,et al.  GLUT1 messenger RNA and protein induction relates to the malignant transformation of cervical cancer. , 2003, American journal of clinical pathology.

[46]  H. Edlund,et al.  Insulin-promoter-factor 1 is required for pancreas development in mice , 1994, Nature.

[47]  Stefan Thor,et al.  Insulin gene enhancer binding protein Isl-1 is a member of a novel class of proteins containing both a homeo-and a Cys–His domain , 1990, Nature.

[48]  A. Zorzano,et al.  Insulin-regulated glucose uptake in rat adipocytes is mediated by two transporter isoforms present in at least two vesicle populations. , 1989, The Journal of biological chemistry.

[49]  O. Warburg.  [Origin of cancer cells]. , 1956, Oncologia.

[50]  J. Russo,et al.  Progressive increase of glucose transporter-3 (GLUT-3) expression in estrogen-induced breast carcinogenesis , 2012, Clinical and Translational Oncology.

[51]  A. Jemal,et al.  Global cancer statistics , 2011, CA: a cancer journal for clinicians.

[52]  S. Weinhouse.  On respiratory impairment in cancer cells. , 1956, Science.