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A1 2.7 a a Sw1990 A2 2.5 a Sw1990 2.6 Panc-1 2.4 a Panc-1 2.5 2.3 2.4 2.3 2��2 2��2 2��1 2��1 2 WST-8 cleavage (absorbance A 450) 2 B1 10 4 P1 P1 10 3 10 2 10 1 10 0 B2 10 4 10 3 10 2 10 1 10 0 miR-95 mimics Mimics-control 10 0 10 1 10 2 10 3 10 4 Annexin V-FITC Sw1990-control 10 0 10 1 10 2 10 3 10 4 Annexin V-FITC Panc-1-control Figure 2 miR-95 promotes cell proliferation (A) and enhancement of miR-95 inhibit apoptosis (B). A total of 10 4 Sw1990 or Panc-1 cells per well were plated in 96-well plates for 24 h and then were transfected with hsa-miR-95 mimics or hsa-miR-95 inhibitor along with paired negative controls. The cells were incubated at 37 ℃ for 48 h and then cell proliferation was assessed using Cell Counting Kit 8. Data were shown as mean ± SD. a P < 0.05 vs pairing negative control. insulin (0.1-1 nmol). Our miRNA real time PCR array showed that high dose glargine (100 IU/L) up-regulated the expression of 10 miRNAs and down-regulated 2 mi- RNAs in Sw1990 pancreatic cancer cells. The most obvious change was the apparent increase of miR-95. Stemloop real-time PCR confirmed the aberrant changes of miR-95 after treatment of high dose glargine in Sw1990 and Panc-1 pancreatic cancer cells. Then miR-95 showed significant anti-apoptotic and growth-promoting effects in vitro and in vivo. Ectopic expression and siRNA knockdown of miR-95 confirmed its invasion-promoting activity in vitro. Therefore, these results highlighted the miR- 95-related changes as important effects of glargine. Recent studies linked the use of glargine with increased risk of cancer. Hemkens et al [4] published a registry study that demonstrated a significantly increased risk of cancer diagnosis associated with high dosages of glargine. However, the Scottish study found a non-significant increased risk for specifically breast cancers [23] . The UK study found no link between glargine and cancer [3] . In addition, although glargine has been shown to increase resistance to apoptosis in several tumor cell lines, administration of WJG|www.wjgnet.com 10 4 10 3 10 2 10 1 10 0 10 4 10 3 10 2 10 1 10 0 WST-8 cleavage (absorbance A 450) 1��9 10 0 10 1 10 2 10 3 10 4 Annexin V-FITC miR-95 mimics 10 0 10 1 10 2 10 3 10 4 Annexin V-FITC miR-95 mimics Li WG et al �� Glargine and pancreatic cancer miR-95 inhibitor Inhibitor-control Percentage o� apoptosis cells (%) Percentage o� apoptosis cells (%) 45 40 35 30 25 20 15 10 5 0 50 40 30 20 10 0 Sw1990-control miR-95 mimics Panc-1-control miR-95 mimics glargine didn’t alter proliferation of Colo-357 pancreatic carcinoma cells in vitro [12] . Therefore, all epidemiological and laboratory evidence remains inconclusive and new indicators are needed to determine the role of glargine in carcinogenesis. miRNAs have been recognized as promising diagnostic and prognostic markers for cancer diagnosis or treatment. For example , miR-34a family members were found to be directly regulated by TP53 and act as tumor suppressors [24] ; miR-217 inhibited pancreatic cancer cell growth through targeting KRAS [25] ; miR-10b promoted pancreatic cancer invasiveness and correlates with a poor prognosis [26] ; The miRNA-200 family (miR-200a, miR-200b, miR-200c, miR-141 and miR-429) were found to inhibit tumor invasion and metastasis by regulating EMT [27] ; miR-126 can inhibit cell adhesion, migration and invasion through the suppression of CRK [28] . Our study confirmed, for the first time, that miR-95 and miR-134 were primary glargineresponsive miRNAs. miR-95 has been shown to be involved in carcinogenesis. A highly characterized example is colorectal carcinoma, in which miR-95 can promote cell proliferation by 2635 June 7, 2012|Volume 18|Issue 21| a a
A Migration Invasion B Migration Invasion Li WG et al �� Glargine and pancreatic cancer miR-95-mimics Sw1990-control Sw1990-control miR-95-inhibitor Figure 3 Effect of miR-95 on tumor cell migration, invasion of Sw1990 cells. A: Invasion and migration assay. Representative fields of invasion (down) or migration (up) cells on the membrane (left, magnification of × 200). Average invasion or migration cell number per field (right). The invasion or migration cell number of Sw1990 transfected with miR-95-mimics drastically increased than that transfected with pairing negative control; B: The invasion or migration cell number of Sw1990 cells transfected with miR-95-inhibitor dramatically decreased than that transfected with pairing negative control. b P < 0.01 vs Sw1990-control, n = 10. regulating sorting Nexin 1 [29] . In pancreatic cancer, miR-95 is significantly upregulated in most tissues and cell lines [30] . In HeLa cells, inhibition of miR-95 caused a decrease in cell growth [31] . miR-134 gene is located at 14q32, and is involved in several physiological and pathological pro- WJG|www.wjgnet.com Sw1990 cell number per field Sw1990 cell number per field 120 100 80 60 40 20 0 120 100 80 60 40 20 0 Sw1990 miR 95 mimics Sw1990-control Migration Invasion cesses. For example, miR-134 plays an important role in translation-dependent guidance of nerve growth cones [32] ; miR-134 is regarded as a potential plasma biomarker for the diagnosis of acute pulmonary embolism [33] ; plasma miR-134 in bipolar disorder serves as a potential periph- 2636 June 7, 2012|Volume 18|Issue 21| b Sw1990 miR 95 inhibitor Sw1990-control b Migration Invasion b b
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World Journal of Gastroenterology W
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Phillip S Oates, Perth Ross C Smith
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Deepak N Amarapurkar, Mumbai Abhiji
Page 7 and 8: Trine Olsen, Tromsø Eyvind J Pauls
Page 9 and 10: Conor P Delaney, Cleveland Sharon D
Page 11 and 12: S Contents EDITORIAL FIELD OF VISIO
Page 13: Contents ACKNOWLEDGMENTS APPENDIX A
Page 19: Cereda S et al . Adjuvant treatment
Page 22 and 23: DM, Sterling RK, Shiffman M, Topaz
Page 25 and 26: Selinger CP et al . Pregnancy relat
Page 31: Selinger CP et al . Pregnancy relat
Page 35 and 36: Ilan Y. Bacterial translocation in
Page 43: Ettreiki C et al . Iron prevents co
Page 46 and 47: A Macroscopir damage scores (AU) 7.
Page 48 and 49: A Total flora 12.5 B Log copy numbe
Page 51 and 52: Ettreiki C et al . Iron prevents co
Page 53: Online Submissions: http://www.wjgn
Page 57: A Fold changes over untreated cells
Page 61 and 62: A miR-95 B Li WG et al �� Glarg
Page 64: Key words: Colorectal cancer; Niger
Page 67 and 68: A HT29 cells 100 C SW116 cells 40 P
Page 69 and 70: A B Ecadherin Vimentin GAPDH Zhou H
Page 71 and 72: Zhou HM et al �� Nigericin and
Page 73 and 74: Terzin V et al . Serum IgG4 in auto
Page 75 and 76: Terzin V et al . Serum IgG4 in auto
Page 77 and 78: Online Submissions: http://www.wjgn
Page 79 and 80: Min YW et al . Sub-centimeter-sized
Page 85: Park CH et al . Family history and
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Page 96 and 97: genetic association study. BMC Canc
Page 98: ed ghrelin levels. World J Gastroen
Page 101 and 102: A Serum acylated ghrelin (pg/mL) B
Page 103 and 104: Yang YJ et al . H. pylori eradicati
Page 105 and 106: Online Submissions: http://www.wjgn
Page 107 and 108: Chen JG et al . Colorectal cancer s
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Chen JG et al . Colorectal cancer s
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Chen JG et al . Colorectal cancer s
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Qiao CX et al . Quality of life wit
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primary liver cancer and one of the
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A A 490 Li YH et al . GABRQ in HCC
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Li YH et al . GABRQ in HCC prostate
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Online Submissions: http://www.wjgn
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Table 1 The main characteristics of
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Shen Y et al . PTEN and cetuximab e
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Shen Y et al . PTEN and cetuximab e
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Yang XX et al . Aberrant methylatio
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Relative expression 10 8 6 4 2 0 1.
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E Methylation (%) F Methylation (%)
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Yang XX et al . Aberrant methylatio
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Di Nardo G et al . Octreotide in pe
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A B Aniwan S et al . Infliximab for
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Aniwan S et al . Infliximab for CD
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Nishizawa T et al . Dual therapy fo
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Nishizawa T et al . Dual therapy fo
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Instructions to authors ISSN and EI
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Instructions to authors AIM (no mor
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Instructions to authors Guidelines
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