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#32705224   2020/06/17 To Up

Parthenolide inhibits human lung cancer cell growth by modulating the IGF‑1R/PI3K/Akt signaling pathway.

Lung cancer is the leading cause of cancer‑associated mortality worldwide. Parthenolide (PTL), a natural product extracted from the plant Tanacetum parthenium, (a flowering plant in the daisy family, Asteraceae) has been reported to inhibit cancer cell growth, including that of human lung cancer. However, the underlying mechanisms by which PTL exerts its anticancer effect have remained to be fully elucidated. In the present study, Cell Counting Kit‑8 and colony formation assays were used to assess the effect of PTL to inhibit cell proliferation, a wound‑healing assay was performed to assess cell migration and western blot analysis and PCR were employed to reveal the molecular mechanisms by which PTL inhibits human lung carcinoma cell growth. The results indicated that PTL substantially inhibited cell proliferation and migration in two lung cancer cell lines A549 and H1299. Mechanistically, the phosphorylation of insulin‑like growth factor 1 receptor (IGF‑1R), Akt and forkhead box O3α (FoxO3α) was blocked by PTL. Furthermore, IGF‑1‑induced Akt [protein kinase B or (PKB)] and FoxO3α phosphorylation were also inhibited by PTL treatment. In addition, PTL significantly suppressed lung cancer growth in a subcutaneous xenograft mouse model. Taken together, the present in vivo and in vitro results indicate that PTL may suppress lung cancer growth through inhibiting IGF‑1R‑mediated PI3K/Akt/FoxO3α signaling, suggesting that PTL may be an attractive candidate for the treatment of lung cancer.
Longhua Sun, Wenxin Yuan, Guilan Wen, Bentong Yu, Fei Xu, Xin Gan, Jianjun Tang, Qinghua Zeng, Lanlan Zhu, Chuanhui Chen, Wei Zhang

2041 related Products with: Parthenolide inhibits human lung cancer cell growth by modulating the IGF‑1R/PI3K/Akt signaling pathway.

1.5x10(6) cells2 Pieces/Box0.1 mg2 Pieces/Box5 x 50 ug450 ug1.5 x 10^6 cells96 wells (1 kit)1.00 flask

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#32705211   2020/07/06 To Up

Lumican mediates HTB94 chondrosarcoma cell growth via an IGF‑IR/Erk1/2 axis.

Chondrosarcoma is a malignant bone tumor characterized by the production of a modified cartilage‑type extracellular matrix (ECM). In the present study, the expression levels of the small leucine‑rich proteoglycans (SLRPs), decorin, biglycan and lumican, were examined in the HTB94 human chondrosarcoma cell line. HTB94 cells were found to express and secrete the 3 SLRP members. RT‑qPCR and western blot analysis demonstrated that lumican was the most abundantly secreted SLRP, whereas decorin and biglycan expression levels were low. The utilization of short interfering RNA specific for the decorin, biglycan, and lumican genes resulted in the efficient downregulation of the respective mRNA levels (P≤0.001). The growth of the HTB94 cells was stimulated by lumican (P≤0.001), whereas their migration and adhesion were not affected (P=NS). By contrast, these cellular functions were not sensitive to a decrease in low endogenous levels of decorin and biglycan. Lumicandeficiency significantly inhibited both basal and insulin‑like growth factor I (IGF‑I)‑induced HTB94 cell growth (P≤0.001 andP≤0.01, respectively). These effects were executed through the insulin‑like growth factor I receptor (IGF‑IR), whose activation was markedly attenuated (P≤0.01) in lumican‑deficient HTB94 cells. The downregulation of lumican induced the substantial inhibition of extracellular regulated kinase (ERK1/2) activation (P≤ 0.01), indicating that ERK1/2 is a necessary component of lumican/IGF‑IR‑mediated HTB94 cell proliferation. Moreover, the lumican‑deficient cells exhibit increased mRNA levels of p53 (P≤0.05), suggesting that lumican facilitates HTB94 cell growth through an IGF‑IR/ERK1/2/p53 signaling cascade. On the whole, the findings of the present study demonstrate that endogenous lumican is a novel regulator of HTB94 cell growth.
Antonis Papoutsidakis, Eirini Maria Giatagana, Aikaterini Berdiaki, Ioanna Spyridaki, Demetrios A Spandidos, Aristidis Tsatsakis, George N Tzanakakis, Dragana Nikitovic

2789 related Products with: Lumican mediates HTB94 chondrosarcoma cell growth via an IGF‑IR/Erk1/2 axis.

100 ug/vial100ug Lyophilized100ug Lyophilized2500 assays100 ug/vial0.1 mg200ul100 µg1 kit0.1 ml

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#32705168   2020/07/02 To Up

miR‑589‑3p sponged by the lncRNA TINCR inhibits the proliferation, migration and invasion and promotes the apoptosis of breast cancer cells by suppressing the Akt pathway via IGF1R.

The long non‑coding (lnc)RNA named tissue differentiation inducing non‑protein coding RNA (TINCR) is a tumor marker that has not been studied in breast cancer. The present study aimed to investigate the TINCR‑targeting micro (mi)RNAs and the regulatory mechanisms of TINCR in breast cancer. Following prediction by TargetScan and confirmation by dual‑luciferase reporter assay, TINCR was demonstrated to be a target gene for miR‑589‑3p. The expression of TINCR and miR‑589‑3p in breast cancer and adjacent tissues was detected by reverse transcription‑quantitative (RT‑q)PCR, and the correlation between TINCR and miR‑589‑3p expression was determined by using Spearman correlation analysis. The 5‑years survival was analyzed in patients with breast cancer according to TINCR expression (high or low). The effects of TINCR and miR‑589‑3p on the proliferation, apoptosis, migratory and invasive abilities of some breast cancer cell lines were detected by MTT assay, flow cytometry, wound healing assay and Transwell assay. The target gene of miR‑589‑3p was predicted and verified by TargetScan and dual‑luciferase reporter assay, and the mechanism of miR‑589‑3p involvement in breast cancer cells was explored by overexpression or downregulation of miR‑589‑3p in breast cancer cells. RT‑qPCR and western blotting were used to determine the expression of the insulin‑like growth factor 1 receptor (IGF1R)/AKT pathway‑related genes. The results demonstrated that TINCR expression level was negatively correlated with miR‑589‑3p expression level in breast cancer tissues and that patients with high expression of TINCR presented with lower survival rates. In addition, TINCR overexpression in cancer cells inhibited miR‑589‑3p expression, and cell transfection with miR‑589‑3p mimic partially reversed the effect of TINCR overexpression on the promotion of cancer cell proliferation, migration and invasion, and on the inhibition of cancer cell apoptosis. Furthermore, IGF1R, which is a target gene of miR‑589‑3p, increased cancer cell proliferation, migration and invasion and inhibited cancer cell apoptosis; however, these effects were partially reversed by miR‑589‑3p mimic. Furthermore, the results demonstrated that miR‑589‑3p mimic could downregulate the protein expression of IGF1R and p‑AKT. In addition, TINCR overexpression downregulated miR‑589‑3p expression level. miR‑589‑3p partially reversed the effects of TINCR overexpression on cancer cell proliferation, migration and invasion, and inhibited cancer cell apoptosis by inhibiting the IGF1R‑Akt pathway. The results from the present study demonstrated that TINCR may sponge miR‑589‑3p in order to inhibit IGF1R‑Akt pathway activation in breast cancer cells, promoting therefore cancer cell proliferation, migration and invasion.
Fangdong Guo, Xiaoyu Zhu, Qingquan Zhao, Qirong Huang

2196 related Products with: miR‑589‑3p sponged by the lncRNA TINCR inhibits the proliferation, migration and invasion and promotes the apoptosis of breast cancer cells by suppressing the Akt pathway via IGF1R.

1 ml200 units1100 1500IU2 Pieces/Boxmin 2 cartons100.00 ul

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#32626989   2020/05/14 To Up

Integrated microarray analysis to identify potential biomarkers and therapeutic targets in dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is a primary cardiomyopathy with high mortality. The aim of the present study was to identify the related genes in DCM. The four expression profiles (GSE17800, GSE21610, GSE42955 and GSE79962) downloaded from the Gene Expression Omnibus (GEO) database were analyzed using RankProd and metaMA R packages to identify differentially expressed genes (DEGs). DEGs were uploaded to the Database for Annotation, Visualization and Integrated Discovery (DAVID), for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. A protein‑protein interaction (PPI) network of the DEGs was constructed using the STRING database. In addition, hub genes were identified using the Cytoscape plugin cytoHubba. A mouse DCM model, which established via intraperitoneal injection with doxorubicin (DOX), was used to validate the hub genes. A total of 898 DEGs were identified across the four microarrays. Furthermore, GO analysis demonstrated that these DEGs were mainly enriched in cell adhesion, negative regulation of cell proliferation, negative regulation of apoptotic process and potassium ion transport. In addition, KEGG analysis revealed that DEGs were mainly enriched in the ECM‑receptor interaction, the p53 signaling pathway, cardiac muscle contraction and the hypoxia‑inducible factor signaling pathway. Proenkephalin (PENK), chordin like 1 (CHRDL1), calumenin (CALU), apolipoprotein L1, insulin‑like growth factor binding protein 3 (IGFBP3) and ceruloplasmin (CP) were identified as hub genes in the PPI network. Furthermore, the expression levels of PENK, CHRDL1, IGFBP3, CP and CALU in hearts with DCM were validated using a mouse model. In conclusion, the present study identified six hub genes related to DCM. Therefore, the present results may provide a potential mechanism for DCM involving these hub genes, which may serve as biomarkers for screening and diagnosis in the clinic.
Hao Zhang, Junyu Huo, Wanying Jiang, Qijun Shan

1751 related Products with: Integrated microarray analysis to identify potential biomarkers and therapeutic targets in dilated cardiomyopathy.

1 module1 module1 module1 module1 module1 module1 module

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#32583001   2020/06/19 To Up

IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway.

Type 1 insulin‑like growth factor receptor (IGF‑IR) signaling is considered to serve a key role in the development of cancer. However, the effects of IGF‑IR on the malignant characteristics of myelodysplastic syndrome (MDS) clonal cells remains to be determined. In the present study it was demonstrated that knockdown of IGF‑IR reduced the proliferation and increased the apoptosis of MDS/leukemia cells. Integrated analysis of gene expression profiles using bioinformatics identified the MAPK signaling pathway as a critical downstream factor of IGF‑IR, and this was confirmed in vitro using western blotting which revealed that IGF‑IR knockdown significantly increased the expression of activated MAPK. Furthermore, IGF‑IR signaling was inhibited to investigate the potential of IGF‑IR as a therapeutic target of MDS. The results revealed that the IGF‑IR inhibitor picropodophyllin (PPP) inhibited cell proliferation, promoted cell apoptosis and arrested the cell cycle at the G2/M phase in MDS/leukemia cells. Similar to the effects of IGF‑IR knockdown, PPP treatment also increased MAPK signaling in vitro. In conclusion, IGF‑IR may serve as a potential therapeutic target of MDS.
Qi He, Qingqing Zheng, Feng Xu, Wenhui Shi, Juan Guo, Zheng Zhang, Sida Zhao, Xiao Li, Chunkang Chang

2258 related Products with: IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway.

2 Pieces/Box2 Pieces/Box2 Pieces/Box100 ml.2 Pieces/Box2 Pieces/Box25 ml.0.5 mg1x10e7 cells

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#32542223   2020/06/05 To Up

Hormonal Contribution to Liver Regeneration.

An understanding of the molecular basis of liver regeneration will open new horizons for the development of novel therapies for chronic liver failure. Such therapies would solve the drawbacks associated with liver transplant, including the shortage of donor organs, long waitlist time, high medical costs, and lifelong use of immunosuppressive agents. Regeneration after partial hepatectomy has been studied in animal models, particularly fumarylacetoacetate hydrolase-deficient () mice and pigs. The process of regeneration is distinctive, complex, and well coordinated, and it depends on the interplay among several signaling pathways (eg, nuclear factor κβ, Notch, Hippo), cytokines (eg, tumor necrosis factor α, interleukin 6), and growth factors (eg, hepatocyte growth factor, epidermal growth factor, vascular endothelial growth factor), and other components. Furthermore, endocrinal hormones (eg, norepinephrine, growth hormone, insulin, thyroid hormones) also can influence the aforementioned pathways and factors. We believe that these endocrinal hormones are important hepatic mitogens that strongly induce and accelerate hepatocyte proliferation (regeneration) by directly and indirectly triggering the activity of the involved signaling pathways, cytokines, growth factors, and transcription factors. The subsequent induction of cyclins and associated cyclin-dependent kinase complexes allow hepatocytes to enter the cell cycle. In this review article, we comprehensively summarize the current knowledge regarding the roles and mechanisms of these hormones in liver regeneration. Articles used for this review were identified by searching MEDLINE and EMBASE databases from inception through June 1, 2019.
Anan A Abu Rmilah, Wei Zhou, Scott L Nyberg

1685 related Products with: Hormonal Contribution to Liver Regeneration.

430 Tests / Kit600 Tests / Kit430 tests1 module1 mgOne 96-Well Strip Micropl250ul 25 G480/kit

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#32473002   2020/05/30 To Up

Coexıstence of Ectopıc Posterıor Pıtuıtary and Sellar/Suprasellar Arachnoıd Cyst: A Case Report.

The ectopic posterior pituitary (EPP) is a rare condition characterized by the ectopic location of posterior pituitary lobe associated with varying degree of stalk anomalies. The arachnoid cysts (AC) are benign lesions of the arachnoid, which account for 1% of all intracranial space-occupying lesions. Sellar/suprasellar ACs account for approximately 1% of all ACs. This is the first case of coexistence EPP with sellar/suprasellar AC.
Suzan Saylisoy, Goknur Yorulmaz

2879 related Products with: Coexıstence of Ectopıc Posterıor Pıtuıtary and Sellar/Suprasellar Arachnoıd Cyst: A Case Report.

100 μg

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#32323783   2020/04/10 To Up

Circular RNA Circ100084 functions as sponge of miR‑23a‑5p to regulate IGF2 expression in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) has become a major cause of cancer‑related mortality worldwide. Circular RNAs (circRNAs) are non‑coding RNAs that serve important roles in multiple cancers. However, the role of circRNAs in HCC remains largely unknown. In the present study, a circRNA microarray dataset of HCC samples, GSE97332, was downloaded from the gene expression omnibus database. Following data preprocessing, differentially expressed circRNAs between HCC tissues and normal tissues were determined using GEO2R. The circRNA‑miRNA interactions were predicted by the miRanda database. The miRTarbase database was used to search for target genes of the miRNAs. A circRNA‑miRNA‑mRNA network was constructed using Cytoscape based on the obtained circRNA, miRNA and mRNA. In this network, the upregulated circRNA hsa_circRNA_100084 was found to be involved in a competing endogenous relationship of hsa_circRNA_100084‑hsa‑miR‑23a‑5p‑ insulin‑like growth factor 2 (IGF2). The differential expression of hsa_circRNA_100084, hsa‑miR‑23a‑5p and IGF2 in HCC tissues and liver cancer cells was validated by reverse transcription‑quantitative PCR. Additionally, the interactions between hsa‑miR‑23a‑5p with hsa_circRNA_100084 and IGF2 were validated by dual‑luciferase reporter assays. Knocking down hsa_circRNA_100084 inhibited the proliferation, migration and invasion of liver cancer cells, while the simultaneous overexpression of IGF2 reversed the effects of hsa_circRNA_100084 knockdown. The results show that hsa_circRNA_100084 could promote the expression of IGF2 by acting as a sponge of hsa‑miR‑23a‑5p in liver cancer cells.
Jie Yang, Ying Li, Zuochun Yu, Yuefen Zhou, Jianfei Tu, Jian Lou, Yonghui Wang

1560 related Products with: Circular RNA Circ100084 functions as sponge of miR‑23a‑5p to regulate IGF2 expression in hepatocellular carcinoma.

1 kit1 kit

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#32030914   2020/02/06 To Up

Low Serum Insulinlike Growth Factor II Levels Correlate with High BMI in American Indian Adults.

Insulinlike growth factor II (IGF-II) regulates metabolism and growth. In humans, both positive and negative relationships have been reported between serum IGF-II levels and obesity. This study assessed the relationship between serum IGF-II levels and BMI and determined whether IGF-II levels predict weight gain.
Yunhua L Muller, Robert L Hanson, Darin Mahkee, Paolo Piaggi, Sayuko Kobes, Wen-Chi Hsueh, William C Knowler, Clifton Bogardus, Leslie J Baier

1760 related Products with: Low Serum Insulinlike Growth Factor II Levels Correlate with High BMI in American Indian Adults.

4 Membranes/Box2 Pieces/Box10ug100.00 ug20ug100.00 ug0.1ml (1mg/ml)Protein100.00 ug100 μg10ug1 kit(96 Wells)

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