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Search results for: IGF II Antisense

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#32070145   // To Up

Long non-coding RNA 91H regulates IGF2 expression by interacting with IGF2BP2 and promotes tumorigenesis in colorectal cancer.

91H, a long non-coding antisense transcripts located on the position of the H19/IGF2 locus had been suggested to play a critical role in tumour development. However, little study had proved the mechanism in colorectal cancer (CRC). Hence, we performed this study to deeply explore the mechanism of lncRNA 91H in tumour progression. The expression of lncRNA 91H was first detected in CRC tissues and cells which was higher and than normal cells or tissues and CRC patients with high lncRNA 91H expression usually had a high risk in tumour metastasis ( < .05). Then, monodansylcadaverine (MDC) staining, scratch wound, migration and invasion assays were conducted which showed to that reduced lncRNA 91H would greatly affect tumour migration, invasion and autophagy. Finally, by RNA pull down and RNA-binding protein immunoprecipitation (RIP) assay, a significant interaction was found between lncRNA 91H and IGF2BP2 which was proved to play an important role in CRC IGF2 expression. All these results suggested lncRNA 91H promotes IGF2 expression by interacting with IGF2BP2 which would provide a new strategy in finding potential CRC diagnostic biomarkers and therapeutic targets.
Tianyi Gao, Xiangxiang Liu, Bangshun He, Yuqin Pan, Shukui Wang

2325 related Products with: Long non-coding RNA 91H regulates IGF2 expression by interacting with IGF2BP2 and promotes tumorigenesis in colorectal cancer.



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#31590432   2019/10/06 To Up

The Neglected Insulin: IGF-II, a Metabolic Regulator with Implications for Diabetes, Obesity, and Cancer.

When originally discovered, one of the initial observations was that, when all of the insulin peptide was depleted from serum, the vast majority of the insulin activity remained and this was due to a single additional peptide, IGF-II. The IGF-II gene is adjacent to the insulin gene, which is a result of gene duplication, but has evolved to be considerably more complicated. It was one of the first genes recognised to be imprinted and expressed in a parent-of-origin specific manner. The gene codes for IGF-II mRNA, but, in addition, also codes for antisense RNA, long non-coding RNA, and several micro RNA. Recent evidence suggests that each of these have important independent roles in metabolic regulation. It has also become clear that an alternatively spliced form of the insulin receptor may be the principle IGF-II receptor. These recent discoveries have important implications for metabolic disorders and also for cancer, for which there is renewed acknowledgement of the importance of metabolic reprogramming.
Jeff M P Holly, Kalina Biernacka, Claire M Perks

1204 related Products with: The Neglected Insulin: IGF-II, a Metabolic Regulator with Implications for Diabetes, Obesity, and Cancer.

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#31317640   2019/07/18 To Up

Long noncoding RNA IGF2AS regulates high-glucose induced apoptosis in human retinal pigment epithelial cells.

High-glucose-induced retinal tissue impairment is the major pathological phenotype of diabetic retinopathy. In an in vitro diabetic apoptosis cell model, we evaluated the function of long noncoding RNA, insulin growth factor 2 antisense (IGF2-AS) in high-glucose-injured human retinal pigment epithelial cells. A human retinal pigment epithelial cell line, ARPE-19 was incubated with high-glucose in vitro to induce apoptosis. SiRNA-mediated IGF2-AS downregulation was conducted in ARPE-19 cells to evaluate its effect on high-glucose induced apoptosis, assessed by a TUNEL assay. qRT-PCR and western blot assays were applied to examine the functional effect of IGF2-AS on IGF2/AKT/Casp-9 expressions in glucose-injured ARPE-19 cells. ART was further knocked down, specifically in IGF2-AS-downregualted ARPE-19 cells, to investigate its functional involvement in IGF2-AS-inhibition-mediated apoptotic protection in glucose-injured ARPE-19 cells. High-glucose induced apoptosis in ARPE-19 cells, and upregulated IGF-2AS in a dose-dependent manner. SiRNA-mediated IGF2-AS downregulation ameliorated apoptosis, upregulated IGF2/AKT and decreased Casp-9, in high-glucose-treated ARPE-19 cells. AKT knockdown was shown to dramatically reverse the preventive effect of IGF2-AS-downregulation on high-glucose-induced apoptosis in ARPE-19 cells. Moreover, it was demonstrated that AKT knockdown directly upregulated Casp-9 in IGF2-AS-downregulated and high-glucose-treated ARPE-19 cells. We demonstrated that inhibiting IGF2-AS, possibly also through activation of AKT signaling pathway, has a protective function in high-glucose-induced apoptosis in human retinal pigment epithelial cells in diabetic retinopathy.
Xiaoyi Yu, Yingzi Luo, Gangyi Chen, Hong Liu, Ni Tian, Xiaoting Zen, Qiuhong Liu

1546 related Products with: Long noncoding RNA IGF2AS regulates high-glucose induced apoptosis in human retinal pigment epithelial cells.

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#30771425   2019/02/14 To Up

Long non-coding RNA FGF13-AS1 inhibits glycolysis and stemness properties of breast cancer cells through FGF13-AS1/IGF2BPs/Myc feedback loop.

LncRNAs have been proven to play crucial roles in various processes of breast cancer. LncRNA FGF13-AS1 has been identified as one of the 25 downregulated lncRNAs in breast cancer through analyzing data from two cohorts and TCGA by another group of our lab. In this study, we report that FGF13-AS1 expression is decreased in breast cancer tissue compared with corresponding normal tissue, and the downregulation of FGF13-AS1 is associated with poor prognosis. Functional studies show that FGF13-AS1 inhibits breast cancer cells proliferation, migration, and invasion by impairing glycolysis and stemness properties. Mechanistically, FGF13-AS1 reduces the half-life of c-Myc (Myc) mRNA by binding RNA-binding proteins, insulin-like growth factor 2 mRNA binding proteins (IGF2BPs) and disrupting the interaction between IGF2BPs and Myc mRNA. Furthermore, Myc transcriptionally inhibits FGF13-AS1, forming a feedback loop in this signaling pathway. These results reveal for the first time that FGF13-AS1 functions as a tumor suppressor by inhibiting glycolysis and stemness properties of breast cancer cells, and the FGF13-AS1/IGF2BPs/Myc feedback loop could be a novel therapeutic target for breast cancer patients.
Fei Ma, Xu Liu, Shibo Zhou, Wenjie Li, Chunxiao Liu, Michelle Chadwick, Cheng Qian

1931 related Products with: Long non-coding RNA FGF13-AS1 inhibits glycolysis and stemness properties of breast cancer cells through FGF13-AS1/IGF2BPs/Myc feedback loop.

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#30423304   2018/11/10 To Up

Long Noncoding RNA IGF2AS is Acting as an Epigenetic Tumor Suppressor in Human Prostate Cancer.

To assess the expression profile and functional mechanism of long noncoding RNA (lncRNA) insulin growth factor 2 antisense (IGF2AS) in human prostate cancer (PCa).
Qiang Chen, Ting Sun, Fang Wang, Binbin Gong, Wenjie Xie, Ming Ma, Xiaorong Yang

1797 related Products with: Long Noncoding RNA IGF2AS is Acting as an Epigenetic Tumor Suppressor in Human Prostate Cancer.

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#29789410   2018/05/22 To Up

A randomised, open-label, parallel group phase 2 study of antisense oligonucleotide therapy in acromegaly.

ATL1103 is a second-generation antisense oligomer targeting the human growth hormone (GH) receptor. This phase 2 randomised, open-label, parallel-group study assessed the potential of ATL1103 as a treatment for acromegaly.
Peter J Trainer, John D C Newell-Price, John Ayuk, Simon J B Aylwin, Aled Rees, William Drake, Philippe Chanson, Thierry Brue, Susan M Webb, Carmen Fajardo, Javier Aller, Ann I McCormack, David J Torpy, George Tachas, Lynne Atley, David Ryder, Martin Bidlingmaier

1043 related Products with: A randomised, open-label, parallel group phase 2 study of antisense oligonucleotide therapy in acromegaly.

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#29649418   2018/04/09 To Up

Roles of progesterone receptor membrane component 1 and membrane progestin receptor alpha in regulation of zebrafish oocyte maturation.

Although previous studies suggest membrane progesterone receptor alpha (mPRα/Paqr7) mediates 17, 20β-dihydroxy-4-pregnen-3-one (DHP) induction of oocyte maturation (OM) in zebrafish, critical information needed to establish mPRα as the receptor mediating OM is lacking. The relative potencies of progestins and specific mPRα agonists in inducing OM matched their relative binding affinities for zebrafish mPRα, supporting its role in OM. Microinjection of pertussis toxin blocked DHP induction of OM and the progestin-induced decrease in cyclic AMP levels, suggesting mPRα activates an inhibitory G protein (Gi). Microinjection of morpholino antisense oligonucleotides to zebrafish pgrmc1 blocked induction of OM by DHP which was accompanied by decreased levels of Pgrmc1 and mPRα on the oocyte plasma membranes. Similarly, treatment of denuded oocytes with a PGRMC1 inhibitor, AG205, blocked the gonadotropin-induced increase in plasma membrane mPRα levels and attenuated DHP induction of OM. Co-incubation with two inhibitors of epidermal growth factor Erbb2, ErbB2 inhibitor II and AG 879, prevented induction of OM by DHP, indicating the likely involvement of Erbb2 in mPRα-mediated signaling. Treatment with AG205 reversed the inhibitory effects of the Erbb2 inhibitors on OM and also inhibited insulin-like growth factor-1 induction of OM. Close associations between Pgrmc1 and mPRα, and between Pgrmc1 and Erbb2 were detected in zebrafish oocytes with in situ proximity ligation assays. The results suggest progestin induction of OM in zebrafish is mediated through an mPRα/Gi/Erbb2 signaling pathway that requires Pgrmc1 for expression of mPRα on oocyte membranes and that Pgrmc1 also is required for induction of OM through Erbb2.
Joseph Aizen, Yefei Pang, Caleb Harris, Aubrey Converse, Yong Zhu, Meagan A Aguirre, Peter Thomas

1935 related Products with: Roles of progesterone receptor membrane component 1 and membrane progestin receptor alpha in regulation of zebrafish oocyte maturation.

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#28472630   2017/05/01 To Up

Eukaryotic initiation factor eIF6 modulates the expression of Kermit 2/XGIPC in IGF- regulated eye development.

The eukaryotic initiation translation factor eIF6 is a highly conserved, essential protein implicated in translation. eIF6 is regulated in vivo by extracellular signals, such as IGF signaling (for a review see Miluzio et al., 2009). In Xenopus, eif6 over-expression causes a delay in eye development (De Marco et al., 2011). In this study we showed that eif6 co-immunoprecipitates with the insulin-like growth factor receptor (igfr) and may function downstream of igf in eye formation. The relationship between eif6 and gipc2, a protein partner of a variety of molecules including membrane proteins, was investigated. gipc2 is required for maintaining igf-induced akt activation on eye development (Wu et al., 2006). Significantly eif6 and gipc2 have opposite effects in eye development. While eif6 is required for eye formation below threshold levels, gipc2 knockdown impairs eye development (De Marco et al., 2011; Wu et al., 2006). In this study, it was shown that in eif6 over-expressors, the delay in eye morphogenesis is reversed by gipc2 injection, while the injection of eif6 down-regulates gipc2 expression. Real-time-PCR indicates that eif6 regulates gipc2 expression in a dose-dependent manner. In contrast, gipc2 knockdown has no significant effect on eif6 mRNA levels. These results suggest that eif6 regulation of gipc2 enables correct morphogenesis of Xenopus eye and stimulate questions on the molecular network implicated in this process.
N De Marco, M Tussellino, R Carotenuto, R Ronca, S Rizzolio, S Biffo, C Campanella

1123 related Products with: Eukaryotic initiation factor eIF6 modulates the expression of Kermit 2/XGIPC in IGF- regulated eye development.

0.1ml (1mg/ml)300 units100.00 ug100 ug100ul1 kit(96 Wells)0.1 mg20 250ul45ug2 Pieces/Box

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#27895308   // To Up

Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2.

Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Although microRNAs are involving in the carcinogenesis and development of pancreatic cancer, little information is known regarding the role of miR-663b in pancreatic cancer. In this study, the expression of miR-663b in pancreatic cancer cells was down-regulated by hypermethylation in its putative promoter region, and overexpression of miR-663b repressed cell proliferation, invasion and migration, and induced apoptosis in pancreatic cancer cells. Bioinformatics analysis, luciferase report assay and rescue experiments showed that insulin-like growth factor 2 (IGF2) was a direct target of miR-663b. Results from clinical samples showed that the expression level of miR-663b correlated with the pathological grading, and the expression of miR-663b was down-regulated and was inversely correlated with IGF2 expression level in pancreatic cancer tissues. More importantly, the long non-coding RNA, HOX transcript antisense RNA (HOTAIR), was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter. Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression. In summary, our studies demonstrated that miR-663b is epigenetically repressed by HOTAIR and exerts its tumor-suppressive function via targeting IGF2 in pancreatic cancer.
Huihua Cai, Yong An, Xuemin Chen, Donglin Sun, Tongbing Chen, Yan Peng, Feng Zhu, Yong Jiang, Xiaozhou He

2170 related Products with: Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2.

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#27780718   2016/10/22 To Up

The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications.

Numerous genomic imprinting loci are regulated by long non-coding RNA (lncRNA). We have previously identified a new lncRNA at the H19/IGF2 locus transcribed in H19 antisense orientation and named 91H. This RNA is conserved among mammals. In mice, 91H regulates positively IGF2 expression from a novel promoter. However, in human the function of 91H at the H19/IGF2 locus remains largely undeciphered. Here, we observed that 91H, H19 and IGF2 are overexpressed in breast tumors. By using 91H-knockdown breast cancer cells, we demonstrated that 91H exerts oncogenic properties by promoting cell growth, migration and invasion as well as tumor growth in xenografted immunodeficient mouse model. Moreover, 91H-knockdown reduces the expression of H19 and IGF2 in breast cancer cells. By chromatin-immunoprecipitation and methylation studies, we found that 91H expression prevents histone and DNA methylation on the maternal allele at the H19/IGF2 locus. These results indicate that 91H, through epigenetic modifications, is responsible of the maintenance of H19/IGF2 genomic imprinting allowing the allele-specific expression of H19 and IGF2. Taken together, overexpression of 91H in breast cancer and 91H-induced epigenetic modifications on H19/IGF2 locus suggest that 91H may play essential role in breast cancer development. Further studies are needed to investigate their role in terms of diagnosis and therapeutic.
Constance Vennin, Nathalie Spruyt, Yves-Marie Robin, Thierry Chassat, Xuefen Le Bourhis, Eric Adriaenssens

2370 related Products with: The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications.

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