scholarly journals Apontic regulates cell proliferation and development by activating the expression of hedgehog and cyclin E

2016 ◽  
Author(s):  
Xian-Feng Wang ◽  
Qian Cheng ◽  
Chong-Lei Fu ◽  
Zi-Zhang Zhou ◽  
Susumu Hirose ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cyclin E ◽  
Tumor Formation ◽  
Promoter Regions ◽  
Evolutionarily Conserved ◽  
Coordinated Expression ◽  
Summary Statement ◽  
Insight Into ◽  
Common Regulator ◽  
Cell Cycle Regulator Cyclin

ABSTRACTHedgehog (Hh) signaling pathway and Cyclin E are key players in cell proliferation and development. Hyperactivation of hh and cyclin E. has been linked to several types of cancer. However, transcriptional regulation of hh and cyclin E. are not well understood. Here we show that an evolutionarily conserved transcription factor Apontic (Apt) is an activator of hh and cyclin E. in Drosophila. Apt directly promotes the expression of hh and cyclin E. through its binding site in the promoter regions of hh and cyclin E. during wing development. This Apt-dependent proper expression of hh and cyclin E. is required for cell proliferation and development of the wing. Apt-mediated expression of hh and cyclin E. can direct proliferation of Hh-expressing cells and simultaneous growth, patterning and differentiation of Hh-recipient cells. The discovery of the coordinated expression of Hh and principal cell-cycle regulator Cyclin E. by Apt implicates insight into the mechanism by which deregulated hh and cyclin E promotes tumor formation.Summary statementWe identified a novel role for Apontic as an important common regulator of the transcription of hedgehog and cyclin E. Our study provides important insights into the mechanism of organ development.

scholarly journals Mad1 Function in Cell Proliferation and Transcriptional Repression Is Antagonized by Cyclin E/CDK2

2005 ◽  
Vol 280 (16) ◽  
pp. 15489-15492 ◽  
Author(s):  
Sabine Rottmann ◽  
Annette R. Menkel ◽  
Caroline Bouchard ◽  
Jürgen Mertsching ◽  
Peter Loidl ◽  
...  
Keyword(s):  
Phase Transition ◽  
Cell Proliferation ◽  
Transcriptional Repression ◽  
Cyclin E ◽  
S Phase ◽  
Cellular Behavior ◽  
Corepressor Complex ◽  
Repressor Complex ◽  
Phase Progression ◽  
Cell Cycle Regulator Cyclin

The transcription factors of the Myc/Max/Mad network play essential roles in the regulation of cellular behavior. Mad1 inhibits cell proliferation by recruiting an mSin3-corepressor complex that contains histone deacetylase activity. Here we demonstrate that Mad1 is a potent inhibitor of the G1to S phase transition, a function that requires Mad1 to heterodimerize with Max and to bind to the corepressor complex. Cyclin E/CDK2, but not cyclin D and cyclin A complexes, fully restored S phase progression. In addition inhibition of colony formation and gene repression by Mad1 were also efficiently antagonized by cyclin E/CDK2. This was the result of cyclin E/CDK2 interfering with the interaction of Mad1 with HDAC1 and reducing HDAC activity. Our findings define a novel interplay between the cell cycle regulator cyclin E/CDK2 and Mad1 and its associated repressor complex and suggests an additional mechanism how cyclin E/CDK2 affects the G1to S phase transition.

scholarly journals Methylmercury elicits rapid inhibition of cell proliferation in the developing brain and decreases cell cycle regulator, cyclin E

2006 ◽  
Vol 27 (6) ◽  
pp. 970-981 ◽  
Author(s):  
Kelly Burke ◽  
Yinghong Cheng ◽  
Baogang Li ◽  
Alex Petrov ◽  
Pushkar Joshi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cyclin E ◽  
Developing Brain ◽  
Cell Cycle Regulator ◽  
Cell Cycle Regulator Cyclin

scholarly journals LINC01089 suppresses lung adenocarcinoma cell proliferation and migration via miR-301b-3p/STARD13 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ye Qian ◽  
Yan Zhang ◽  
Haoming Ji ◽  
Yucheng Shen ◽  
Liangfeng Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
High Morbidity ◽  
Lipid Transfer ◽  
Protein Coding ◽  
Cell Proliferation And Migration ◽  
Reduce Cell Proliferation ◽  
And Migration ◽  
Insight Into ◽  
Proliferation And Migration

Abstract Background Lung adenocarcinoma (LUAD) is one of the most common cancers with high morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) serve as tumor promoters or suppressors in the development of various human malignancies, including LUAD. Although long intergenic non-protein coding RNA 1089 (LINC01089) suppresses the progression of breast cancer, its mechanism in LUAD requires further exploration. Thus, we aimed to investigate the underlying function and mechanism of LINC01089 in LUAD. Methods The expression of LINC01089 in LUAD and normal cell lines was detected. Functional assays were applied to measure cell proliferation, apoptosis and migration. Besides, mechanism experiments were employed for assessing the interplay among LINC01089, miR-301b-3p and StAR related lipid transfer domain containing 13 (STARD13). Data achieved in this study was statistically analyzed with Student’s t test or one-way analysis of variance. Results LINC01089 expression was significantly down-regulated in LUAD tissues and cells and its overexpression could reduce cell proliferation and migration. Moreover, LINC01089 could regulate STARD13 expression through competitively binding to miR-301b-3p in LUAD. Additionally, rescue assays uncovered that STARD13 depletion or miR-301b-3p overexpression could countervail the restraining effect of LINC01089 knockdown on the phenotypes of LUAD cells. Conclusion LINC01089 served as a tumor-inhibitor in LUAD by targeting miR-301b-3p/STARD13 axis, providing an innovative insight into LUAD therapies. Trial registration Not applicable.

scholarly journals The Coordinated Upregulated Expression of Genes Involved in MEP, Chlorophyll, Carotenoid and Tocopherol Pathways, Mirrored the Corresponding Metabolite Contents in Rice Leaves during De-Etiolation

Plants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1456
Author(s):  
Xin Jin ◽  
Can Baysal ◽  
Margit Drapal ◽  
Yanmin Sheng ◽  
Xin Huang ◽  
...  
Keyword(s):  
Higher Plants ◽  
Expression Patterns ◽  
Regulatory Elements ◽  
Isoprenoid Biosynthesis ◽  
Promoter Regions ◽  
Expression Of Genes ◽  
Coordinated Expression ◽  
Rice Leaves ◽  
Mechanistic Basis ◽  
Phosphate Synthase

Light is an essential regulator of many developmental processes in higher plants. We investigated the effect of 4-hydroxy-3-methylbut-2-enyl diphosphate reductase 1/2 genes (OsHDR1/2) and isopentenyl diphosphate isomerase 1/2 genes (OsIPPI1/2) on the biosynthesis of chlorophylls, carotenoids, and phytosterols in 14-day-old etiolated rice (Oyza sativa L.) leaves during de-etiolation. However, little is known about the effect of isoprenoid biosynthesis genes on the corresponding metabolites during the de-etiolation of etiolated rice leaves. The results showed that the levels of α-tocopherol were significantly increased in de-etiolated rice leaves. Similar to 1-deoxy-D-xylulose-5-phosphate synthase 3 gene (OsDXS3), both OsDXS1 and OsDXS2 genes encode functional 1-deoxy-D-xylulose-5-phosphate synthase (DXS) activities. Their expression patterns and the synthesis of chlorophyll, carotenoid, and tocopherol metabolites suggested that OsDXS1 is responsible for the biosynthesis of plastidial isoprenoids in de-etiolated rice leaves. The expression analysis of isoprenoid biosynthesis genes revealed that the coordinated expression of the MEP (2-C-methyl-D-erythritol 4-phosphate) pathway, chlorophyll, carotenoid, and tocopherol pathway genes mirrored the changes in the levels of the corresponding metabolites during de-etiolation. The underpinning mechanistic basis of coordinated light-upregulated gene expression was elucidated during the de-etiolation process, specifically the role of light-responsive cis-regulatory motifs in the promoter region of these genes. In silico promoter analysis showed that the light-responsive cis-regulatory elements presented in all the promoter regions of each light-upregulated gene, providing an important link between observed phenotype during de-etiolation and the molecular machinery controlling expression of these genes.

scholarly journals Sevoflurane inhibits malignant progression of colorectal cancer via hsa_circ_0000231-mediated miR-622

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Jingpeng Wang ◽  
Shuyuan Li ◽  
Gaofeng Zhang ◽  
Huihua Han
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Volatile Anesthetic ◽  
Tumor Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas

Abstract Background Sevoflurane (Sev), a commonly used volatile anesthetic, has been reported to inhibit the process of colorectal cancer (CRC). Circular RNAs (circRNAs) are revealed to participate in the pathogenesis of CRC. This study aims to reveal the mechanism of hsa_circ_0000231 in Sev-mediated CRC progression. Methods The expression of hsa_circ_0000231 and microRNA-622 (miR-622) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Protein level was determined by western blot analysis. Cell proliferation was investigated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), cell colony formation and DNA content quantitation assays. Cell apoptosis was detected by Annexin V-fluorescein isothiocyanate and propidium iodide double staining and caspase 3 activity assays. Cell migration and invasion were investigated by wound-healing and transwell invasion assays, respectively. The putative relationship between hsa_circ_0000231 and miR-622 was predicted by circular RNA Interactome online database, and identified by dual-luciferase reporter and RNA immunoprecipitation assays. The impacts of hsa_circ_0000231 on Sev-mediated tumor formation in vivo were presented by in vivo assay. Results Hsa_circ_0000231 expression was upregulated, while miR-622 was downregulated in CRC tissues and cells compared with control groups. Sev treatment decreased hsa_circ_0000231 expression, but increased miR-622 expression in CRC cells. Sev treatment suppressed cell proliferation, migration and invasion, and induced cell apoptosis. Hsa_circ_0000231 overexpression restored Sev-mediated CRC progression in vitro. Additionally, hsa_circ_0000231 acted as a sponge of miR-622, and miR-622 inhibitors reversed the impacts of hsa_circ_0000231 silencing on CRC process. Furthermore, Sev treatment inhibited tumor growth by regulating hsa_circ_0000231 in vivo. Conclusion Hsa_circ_0000231 attenuated Sev-aroused repression impacts on CRC development by sponging miR-622. This findings may provide an appropriate anesthetic protocol for CRC sufferers undergoing surgery.

Systematic discovery and characterization of stress-related microRNA genes in Oryza sativa

Biologia ◽  
2015 ◽  
Vol 70 (1) ◽  
Author(s):  
Kai Bin Xie ◽  
Xue Zhou ◽  
Tian Hai Zhang ◽  
Bao Long Zhang ◽  
Li Ming Chen ◽  
...  
Keyword(s):  
Abiotic Stress ◽  
Stress Responses ◽  
Systematic Investigation ◽  
Chemical Toxicity ◽  
Promoter Regions ◽  
Crop Species ◽  
Translation Inhibition ◽  
Microrna Genes ◽  
Insight Into

AbstractAbiotic stresses including drought, salinity, extreme temperatures, chemical toxicity and oxidative are the natural status of the environment to exert serious threats to agriculture. Abiotic stress-related microRNAs (ASmiRNAs) are a group of microRNAs (miRNAs) regulating stress responses in plants. However, the systematic investigation of ASmiRNAs is limited in Rice (O. sativa), a typical abiotic stress-resistant crop species. In the present work, we systematically investigated ASmiRNAs in silico. First, we identified 177 putative ASmiRNAs in O.sativa. Second, we found most ASmiRNAs were driven by TATA-promoter and most stress-related miRNA promoter regions contained the stress-related elements. Third, we found many ASmiRNAs families were species/family specific and a set of miRNAs might derive from genomic repeat-sequences in O. sativa. Finally, we found the ASmiRNAs in O. sativa target 289 genes with 1050 predicted target sites in which 98% sites have cleavage activity and 2% sites have translation inhibition activity. In conclusion, our findings provide an insight into both the function and evolution of ASmiRNAs and improve our understanding on the mechanism of abiotic stress resistance in O. sativa.

NF-κB inducible genes BCL-X and cyclin E promote immature B-cell proliferation and survival

2004 ◽  
Vol 232 (1-2) ◽  
pp. 9-20 ◽  
Author(s):  
Biao Feng ◽  
Shuhua Cheng ◽  
Constance Yu Hsia ◽  
Leslie B. King ◽  
John G. Monroe ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Cyclin E ◽  
Inducible Genes

scholarly journals Oncogenes - the basics

2018 ◽  
Vol 3 (4) ◽  
pp. 35-37
Author(s):  
Arnab Ghosh ◽  
Diasma Ghartimagar ◽  
Sushma Thapa
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Normal Cell ◽  
Tumor Formation ◽  
Precursor Cell ◽  
Single Precursor ◽  
Normal Cell Cycle

Normal cell cycle and cell proliferation are regulated by several genes which can be broadly classified into 4 groups viz, proto-oncogenes, tumor suppressor genes, genes regulating apoptosis and genes involved in DNA repair. These genes may be defective due to different factors. The defective genes may lead to production of abnormal proteins which may lead to disruption of the normal cell cycle and proliferation. A single precursor cell with defective gene proliferates surpassing the normal physiologic regulatory process and leads to tumor formation, so, traditionally,it is said that “tumors are clonal”.

Cell proliferation is insufficient, but loss of tuberin is necessary, for chemically induced nephrocarcinogenicity

2002 ◽  
Vol 283 (2) ◽  
pp. F262-F270 ◽  
Author(s):  
Hae-Seong Yoon ◽  
Terrence J. Monks ◽  
Jeffrey I. Everitt ◽  
Cheryl L. Walker ◽  
Serrine S. Lau
Keyword(s):  
Cell Proliferation ◽  
Tissue Injury ◽  
Tumor Development ◽  
Suppressor Gene ◽  
Tumor Formation ◽  
Renal Tumors ◽  
Outer Stripe ◽  
Acute Tissue Injury ◽  
Cell Cycle Deregulation ◽  
Erk Activity

Although 2,3,5-tris-(glutathion- S-yl)hydroquinone (TGHQ; 2.5 μmol/kg ip) markedly increased cell proliferation within the outer stripe of the outer medulla (OSOM) of the kidney in both wild-type ( Tsc2+/+ ) and mutant Eker rats ( Tsc2 EK/+), only TGHQ-treated Tsc2 EK/+ rats developed renal tumors, indicating that cell proliferation per se was not sufficient for tumor development. Tuberin expression was initially induced within the OSOM after TGHQ treatment but was lost within TGHQ-induced renal tumors. High extracellular signal-regulated kinase (ERK) activity occurred in the OSOM of Tsc2 EK/+ rats at 4 mo and in TGHQ-induced renal tumors. Cyclin D1 was also highly expressed in TGHQ-induced renal tumors. Reexpression of Tsc2 in tuberin-negative cells decreased ERK activity, consistent with the growth-suppressive effects of this tumor suppressor gene. Thus 1) stimulation of cell proliferation after toxicant insult is insufficient for tumor formation; 2) tuberin induction after acute tissue injury suggests that Tsc2 is an acute-phase response gene, limiting the proliferative response after injury; and 3) loss of Tsc2 gene function is associated with cell cycle deregulation.

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