Galectin genes: Regulation of expression

Chiariotti, Lorenzo; Salvatore, Paola; Frunzio, Rodolfo; Bruni, Carmelo B.

doi:10.1023/b:glyc.0000014073.23096.3a

Cited by 86 publications

(64 citation statements)

References 69 publications

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“…[13][14][15] Therefore we hypothesized that DNMTs may be involved in CPT-induced signaling. The time course of DNMT protein levels after CPT treatment is shown in Fig.…”

Section: Confirmation Of Galectin-1 Identificationmentioning

confidence: 99%

Camptothecin-Induced Cell Proliferation Inhibition and Apoptosis Enhanced by DNA Methyltransferase Inhibitor, 5-Aza-2'-deoxycytidine

Ding

Qiu

Zhang

et al. 2009

Biological & Pharmaceutical Bulletin

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Camptothecin (CPT) was originally isolated from the bark of the Chinese tree, Camptotheca acuminate (Nyssaceae family), and is a DNA topoisomerase I (Top1) inhibitor that reversibly binds to Top1 cleavage complexes (Top1ccs). Several CPT derivatives are now commonly used in the treatment of certain human cancers, especially hepatocellular carcinoma.1,2) The conversion of Top1ccs into irreversible Top1 covalent complexes results in DNA damage, induction of DNA repair mechanisms, and changes in expression for cellcycle proteins related to growth arrest and apoptosis; defects in key factors of these pathways are essential to the oncogenic process and related to the effects of Top 1 inhibitors. For example, CPT can activate poly(ADP-ribose) polymerase (PARP), which is involved in DNA-repair mechanisms and plays a crucial role in maintaining gene stability.3) PARP-deficient and knockout cells have been shown hypersensitive to CPT and more susceptible to oncogenic transformation. 4)Furthermore, administration of a PARP inhibitor increased the anti-tumor activity of CPT derivatives in a mouse model. 5) Inhibitors of CHK1, 6,7) CHK2, 8) and nuclear factor (NF)-kB, 9) which are involved in CPT-induced cellular pathways, have also shown enhanced cytotoxicity when combined with CPT treatment.Regulation of CHK1, CHK2, and NF-kB has extended the application of CPT to other disease states and produced promising results in several cancer clinical trials.10) Nevertheless, further studies are necessary to discover additional factors involved in CPT-induced cellular responses. We analyzed several common gene expression patterns in four human tumor cell lines exposed to CPT using cDNA microarrays and found that multiple intracellular pathways were activated.11) The goal of the present study was to use proteomics to identify proteins that change expression following treatment with CPT in the hepatocellular carcinoma cell line, SMMC-7721. We hypothesize that proteomic profiling may be useful to classify protein expression patterns of tumors with activated signaling pathways that would be sensitive to CPT. This type of study has the potential to develop molecular readouts of tumor signaling pathways so as to optimize therapies for rapid and effective treatment of specific types of cancer. MATERIALS AND METHODS Cell Culture and Cell Viability AssaysThe human hepatocellular carcinoma cell line, SMMC-7721, was obtained from the Department of Biochemistry of the Second Military Medical University, Shanghai, China. Cell viability after treatment of CPT was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Cells were treated with dilutions of CPT of 1.36-330 mg/ml, cultured for 72 h, incubated with 250 mg/ml MTT for 4 h, and analyzed by microplate reader. For CPT and 5-aza-2Ј-deoxycytidine (DAC) co-treatment, cells were treated with 0.1 mM freshly prepared DAC. Treatment was replenished every 24 h and after 72 h, cells were washed with phosphae buffered saline (PBS) then incubated in drug-free media...

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“…[13][14][15] Therefore we hypothesized that DNMTs may be involved in CPT-induced signaling. The time course of DNMT protein levels after CPT treatment is shown in Fig.…”

Section: Confirmation Of Galectin-1 Identificationmentioning

confidence: 99%

Camptothecin-Induced Cell Proliferation Inhibition and Apoptosis Enhanced by DNA Methyltransferase Inhibitor, 5-Aza-2'-deoxycytidine

Ding

Qiu

Zhang

et al. 2009

Biological & Pharmaceutical Bulletin

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show abstract

“…Mammalian galectin-1s are reported to be regulated by various signal pathways (Chiariotti et al, 2002). However, the regulation of fish Pdlgals1 expression has not been fully characterized.…”

Section: Discussionmentioning

confidence: 99%

Molecular characterization of the lgals1 gene in large scale loach Paramisgurnus dabryanus

Zhou

Long

Song

et al. 2016

Gene

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“…It was found that the majority of them have a certain structure responsible for recognition, therefore creation of high affinity compounds allows them to be used as vectors for directed drug transport. [11] …”

Section: Application Of Macromolecules With Carbohydrate Residuesmentioning

confidence: 99%

Macromolecules with Сarbohydrate Residues and Their Application in Glycobiology, Biotechnology and Material Science

Bolsheborodova¹,

Sebyakin²

2012

MHC

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Galectin genes: Regulation of expression

Cited by 86 publications

References 69 publications

Camptothecin-Induced Cell Proliferation Inhibition and Apoptosis Enhanced by DNA Methyltransferase Inhibitor, 5-Aza-2'-deoxycytidine

Camptothecin-Induced Cell Proliferation Inhibition and Apoptosis Enhanced by DNA Methyltransferase Inhibitor, 5-Aza-2'-deoxycytidine

Molecular characterization of the lgals1 gene in large scale loach Paramisgurnus dabryanus

Macromolecules with Сarbohydrate Residues and Their Application in Glycobiology, Biotechnology and Material Science

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