scholarly journals SLC26A2 gene expression levels in melanoma

2021 ◽  
Vol 31 (Supplement_2) ◽  
Author(s):  
Diana Assis ◽  
Ana Luísa De Sousa-Coelho
Keyword(s):  
Gene Expression ◽  
Cancer Cells ◽  
Normal Skin ◽  
Braf Inhibitor ◽  
Ovarian Cancer Cells ◽  
Data Sets ◽  
Dependent Manner ◽  
Therapeutic Decisions ◽  
Pharmacological Screening ◽  
And Function

Abstract Background A recent repurposing pharmacological screening revealed that vanadium-containing drugs anti-proliferative action in ovarian cancer cells was SLC26A2-dependent. SLC26A2/DTDST is a sulfate transporter, related to chondrodysplasia syndromes. Despite some reports on colon cancer, there are no studies on SLC26A2 performed in melanoma in the literature. Methods To better understand its potential use as biomarker for therapeutic decisions in melanoma, we performed gene expression analyses of the data available at GEO profiles (NCBI). Gene data sets that allowed analysis of SLC26A2 expression (1) in melanoma; (2) in response to drugs; (3) regulated by other proteins, were selected. Results Our results showed that, compared to normal skin or benign nevi, SLC26A2 expression was 2.5-fold higher in malignant melanoma (P = 0.019). Compared to the primary tumor, SLC26A2 expression tripled in melanoma (P = 0.022). We found a 6% decrease of SLC26A2 expression in A375 melanoma cells treated with BRAF inhibitor Vemurafenib (P < 0.001). After treatment of A375 cells with MLN4924, a selective inhibitor of the activating enzyme of Nedd8, SLC26A2 decreased in a time-dependent manner ( > 80% at 24 h; P < 0.001). In Sk-Mel-2 cells overexpressing E2F-1, a transcription factor that induces apoptosis in cancer cells, SLC26A2 levels were reduced by 76.4% (P = 0.067). In A375P cells depleted of PGC1α, an important metabolic co-activator in mitochondrial biogenesis and function, SLC26A2 levels increased 16% (P = 0.013). Conclusions From this work, we unveiled, for the first time, potential clues to better understand the regulation and role of SLC26A2 in melanoma. Though, it is still to be determined whether SLC26A2 is a driver or a passenger in the disease.

scholarly journals Formation and Composition of the Bacillus anthracis Endospore

2004 ◽  
Vol 186 (1) ◽  
pp. 164-178 ◽  
Author(s):  
Hongbin Liu ◽  
Nicholas H. Bergman ◽  
Brendan Thomason ◽  
Shamira Shallom ◽  
Alyson Hazen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bacillus Anthracis ◽  
Dna Microarrays ◽  
Data Sets ◽  
Dependent Manner ◽  
Anthrax Spores ◽  
Complementary Nature ◽  
And Function ◽  
Protective Proteins ◽  
Physical Construction

ABSTRACT The endospores of Bacillus anthracis are the infectious particles of anthrax. Spores are dormant bacterial morphotypes able to withstand harsh environments for decades, which contributes to their ability to be formulated and dispersed as a biological weapon. We monitored gene expression in B. anthracis during growth and sporulation using full genome DNA microarrays and matched the results against a comprehensive analysis of the mature anthrax spore proteome. A large portion (∼36%) of the B. anthracis genome is regulated in a growth phase-dependent manner, and this regulation is marked by five distinct waves of gene expression as cells proceed from exponential growth through sporulation. The identities of more than 750 proteins present in the spore were determined by multidimensional chromatography and tandem mass spectrometry. Comparison of data sets revealed that while the genes responsible for assembly and maturation of the spore are tightly regulated in discrete stages, many of the components ultimately found in the spore are expressed throughout and even before sporulation, suggesting that gene expression during sporulation may be mainly related to the physical construction of the spore, rather than synthesis of eventual spore content. The spore also contains an assortment of specialized, but not obviously related, metabolic and protective proteins. These findings contribute to our understanding of spore formation and function and will be useful in the detection, prevention, and early treatment of anthrax. This study also highlights the complementary nature of genomic and proteomic analyses and the benefits of combining these approaches in a single study.

scholarly journals Guizhi Fuling Wan, a Traditional Chinese Herbal Formula, Sensitizes Cisplatin-Resistant Human Ovarian Cancer Cells through Inactivation of the PI3K/AKT/mTOR Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Li Han ◽  
Xiaojuan Guo ◽  
Hua Bian ◽  
Lei Yang ◽  
Zhong Chen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Mtor Pathway ◽  
Cell Counting ◽  
Ovarian Cancer Cells ◽  
Dependent Manner ◽  
Bioactive Constituents ◽  
Anticancer Efficacy ◽  
Protein Levels ◽  
And Function

The aim of the study was to explore the possible mechanisms that Guizhi Fuling Wan (GFW) enhances the sensitivity of the SKOV3/DDP ovarian cancer cells and the resistant xenograft tumours to cisplatin. Rat medicated sera containing GFW were prepared by administering GFW to rats, and the primary bioactive constituents of the sera were gallic acid, paeonol, and paeoniflorin analysed by HPLC/QqQ MS. Cell counting kit-8 analysis was shown that coincubation of the sera with cisplatin/paclitaxel enhanced significantly the cytotoxic effect of cisplatin or paclitaxel in SKOV3/DDP cells. The presence of the rat medicated sera containing GFW resulted in an increase in rhodamine 123 accumulation by flow cytometric assays and a decrease in the protein levels of P-gp, phosphorylation of AKT at Ser473, and mTOR in a dose-dependent manner in SKOV3/DDP cells by western blot analysis, but the sera had no effect on the protein levels of PI3K p110αand total AKT. The low dose of GFW enhanced the anticancer efficacy of cisplatin and paclitaxel treatment in resistant SKOV3/DDP xenograft tumours. GFW could sensitize cisplatin-resistant SKOV3/DDP cells by inhibiting the protein level and function of P-gp, which may be medicated through inactivation of the PI3K/AKT/mTOR pathway.

scholarly journals Propofol suppresses cell viability, cell cycle progression and motility and induces cell apoptosis of ovarian cancer cells through suppressing MEK/ERK signaling via targeting circVPS13C/miR-145 axis

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Huan Lu ◽  
Guanlin Zheng ◽  
Xiang Gao ◽  
Chanjuan Chen ◽  
Min Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cancer Cells ◽  
Rna Binding ◽  
Erk Signaling ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Dependent Manner ◽  
Vacuolar Protein

Abstract Background Propofol is a kind of common intravenous anaesthetic agent that plays an anti-tumor role in a variety of cancers, including ovarian cancer. However, the working mechanism of Propofol in ovarian cancer needs further exploration. Methods The viability and metastasis of ovarian cancer cells were assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell assays. Flow cytometry was used to evaluate the cell cycle and apoptosis. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the abundance of circular RNA vacuolar protein sorting 13 homolog C (circVPS13C) and microRNA-145 (miR-145). The target relationship between miR-145 and circVPS13C was predicted by circinteractome database and verified by dual-luciferase reporter assay, RNA-binding protein immunoprecipitation (RIP) assay and RNA-pull down assay. Western blot assay was used to detect the levels of phosphorylated extracellular regulated MAP kinase (p-ERK), ERK, p-MAP kinse-ERK kinase (p-MEK) and MEK, in ovarian cancer cells. Results Propofol treatment suppressed the viability, cell cycle and motility and elevated the apoptosis rate of ovarian cancer cells. Propofol up-regulated miR-145 in a dose-dependent manner. Propofol exerted an anti-tumor role partly through up-regulating miR-145. MiR-145 was a direct target of circVPS13C. Propofol suppressed the progression of ovarian cancer through up-regulating miR-145 via suppressing circVPS13C. Propofol functioned through circVPS13C/miR-145/MEK/ERK signaling in ovarian cancer cells. Conclusion Propofol suppressed the proliferation, cell cycle, migration and invasion and induced the apoptosis of ovarian cancer cells through circVPS13C/miR-145/MEK/ERK signaling in vitro.

scholarly journals Gene Expression and Transcriptome Profiling of Changes in a Cancer Cell Line Post-Exposure to Cadmium Telluride Quantum Dots: Possible Implications in Oncogenesis

Dose-Response ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 155932582110198
Author(s):  
Mohammed S. Aldughaim ◽  
Mashael R. Al-Anazi ◽  
Marie Fe F. Bohol ◽  
Dilek Colak ◽  
Hani Alothaid ◽  
...  
Keyword(s):  
Gene Expression ◽  
Quantum Dots ◽  
Cancer Cells ◽  
Cadmium Telluride ◽  
Cancer Progression ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Dependent Manner ◽  
Cdte Qds ◽  
Cadmium Telluride Quantum Dots

Cadmium telluride quantum dots (CdTe-QDs) are acquiring great interest in terms of their applications in biomedical sciences. Despite earlier sporadic studies on possible oncogenic roles and anticancer properties of CdTe-QDs, there is limited information regarding the oncogenic potential of CdTe-QDs in cancer progression. Here, we investigated the oncogenic effects of CdTe-QDs on the gene expression profiles of Chang cancer cells. Chang cancer cells were treated with 2 different doses of CdTe-QDs (10 and 25 μg/ml) at different time intervals (6, 12, and 24 h). Functional annotations helped identify the gene expression profile in terms of its biological process, canonical pathways, and gene interaction networks activated. It was found that the gene expression profiles varied in a time and dose-dependent manner. Validation of transcriptional changes of several genes through quantitative PCR showed that several genes upregulated by CdTe-QD exposure were somewhat linked with oncogenesis. CdTe-QD-triggered functional pathways that appear to associate with gene expression, cell proliferation, migration, adhesion, cell-cycle progression, signal transduction, and metabolism. Overall, CdTe-QD exposure led to changes in the gene expression profiles of the Chang cancer cells, highlighting that this nanoparticle can further drive oncogenesis and cancer progression, a finding that indicates the merit of immediate in vivo investigation.

scholarly journals Effect of estrogen receptor β agonists on proliferation and gene expression of ovarian cancer cells

BMC Cancer ◽  
2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Susanne Schüler-Toprak ◽  
Christoph Moehle ◽  
Maciej Skrzypczak ◽  
Olaf Ortmann ◽  
Oliver Treeck
Keyword(s):  
Gene Expression ◽  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Estrogen Receptor Β ◽  
Ovarian Cancer Cells

Bile acids upregulate BRCA1 and downregulate estrogen receptor 1 gene expression in ovarian cancer cells

2018 ◽  
Vol 27 (6) ◽  
pp. 553-556 ◽  
Author(s):  
Qunyan Jin ◽  
Olivier Noel ◽  
Mai Nguyen ◽  
Lionel Sam ◽  
Glenn S. Gerhard
Keyword(s):  
Gene Expression ◽  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Bile Acids ◽  
Ovarian Cancer Cells ◽  
Estrogen Receptor 1

scholarly journals Pharmacologically targeting tribbles gene expression in colorectal cancer

2021 ◽  
Vol 31 (Supplement_2) ◽  
Author(s):  
Victor Yassuda ◽  
Ana Luísa De Sousa-Coelho
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Cell Types ◽  
Disease Recurrence ◽  
Rosemary Extract ◽  
Acid Oxidation ◽  
Data Sets ◽  
Compensatory Mechanism ◽  
Dependent Manner ◽  
Pharmacological Potential

Abstract Background TRIB1, TRIB2 and TRIB3 belong to the mammalian Tribbles family of pseudokinases proteins. Several studies reported Tribbles oncogenic role in different types of cancer, including colorectal cancer (CRC). Though current CRC treatment can be curative, patients are in risk of disease recurrence, meaning novel pharmacological targets and strategies are required. Our goal was to analyze Tribbles gene expression in CRC in response to different drugs. Methods Tribbles transcript levels were obtained from GEO profiles database (NCBI). Gene data sets (GDS) were selected based on experimental drug treatment description. Statistical analysis was performed at GraphPadPrism. Results Compared to non-treated control, TRIB2 expression was ∼2-fold increased in colorectal adenocarcinoma samples from patients treated with cyclooxygenase-2 inhibitor celecoxib (GDS3384), though not statistically significant (P < 0.1). TRIB1 was unaltered and data for TRIB3 was not available. By contrast, all Tribbles showed differential expression after treatment of SW620 colon cancer cells with supercritical rosemary extract in progressive increasing doses (0, 30, 60, 100 μg/mL) (P < 0.01;GDS5416). While both TRIB1 and TRIB3 were moderately increased in a dose-dependent manner (∼18% and 13%, respectively), TRIB2 was maximally down-regulated by ∼15% after 60 μg/mL. Conclusions Although celecoxib exhibits antiproliferative effects in different cancer cell types, TRIB2 gene expression showed a trend to be induced after treatment, in contrast to several genes involved in fatty acid oxidation that were down-regulated, which could result from a compensatory mechanism based on a metabolic shift. Since TRIB1/TRIB3 and TRIB2 were oppositely modulated in response to rosemary extract, additional studies are needed to validate its specific pharmacological potential interest for CRC treatment.

S2039 The Effect of Altering Trefoil Factor-3 (TFF3) Expression On Gene Expression and Function in Human Gastrointestinal Cancer Cells

2009 ◽  
Vol 136 (5) ◽  
pp. A-318
Author(s):  
Hisayuki Matsunaga ◽  
Xiuliang Bao ◽  
Lawrence Werther ◽  
Soichiro Miura ◽  
Steven H. Itzkowitz
Keyword(s):  
Gene Expression ◽  
Cancer Cells ◽  
Gastrointestinal Cancer ◽  
Trefoil Factor ◽  
Trefoil Factor 3 ◽  
And Function

scholarly journals Activating Hippo Pathway via Rassf1 by Ursolic Acid Suppresses the Tumorigenesis of Gastric Cancer

2019 ◽  
Vol 20 (19) ◽  
pp. 4709 ◽  
Author(s):  
Seong-Hun Kim ◽  
Hua Jin ◽  
Ruo Yu Meng ◽  
Da-Yeah Kim ◽  
Yu Chuan Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cancer Cells ◽  
Ursolic Acid ◽  
Hippo Pathway ◽  
Dependent Manner ◽  
Gastric Cancer Cells ◽  
Protein Levels ◽  
Tumor Tissues ◽  
The Hippo Pathway

The Hippo pathway is often dysregulated in many carcinomas, which results in various stages of tumor progression. Ursolic acid (UA), a natural compound that exists in many herbal plants, is known to obstruct cancer progression and exerts anti-carcinogenic effect on a number of human cancers. In this study, we aimed to examine the biological mechanisms of action of UA through the Hippo pathway in gastric cancer cells. MTT assay showed a decreased viability of gastric cancer cells after treatment with UA. Following treatment with UA, colony numbers and the sizes of gastric cancer cells were significantly diminished and apoptosis was observed in SNU484 and SNU638 cells. The invasion and migration rates of gastric cancer cells were suppressed by UA in a dose-dependent manner. To further determine the gene expression patterns that are related to the effects of UA, a microarray analysis was performed. Gene ontology analysis revealed that several genes, such as the Hippo pathway upstream target gene, ras association domain family (RASSF1), and its downstream target genes (MST1, MST2, and LATS1) were significantly upregulated by UA, while the expression of YAP1 gene, together with oncogenes (FOXM1, KRAS, and BATF), were significantly decreased. Similar to the gene expression profiling results, the protein levels of RASSF1, MST1, MST2, LATS1, and p-YAP were increased, whereas those of CTGF were decreased by UA in gastric cancer cells. The p-YAP expression induced in gastric cancer cells by UA was reversed with RASSF1 silencing. In addition, the protein levels in the Hippo pathway were increased in the UA-treated xenograft tumor tissues as compared with that in the control tumor tissues; thus, UA significantly inhibited the tumorigenesis of gastric cancer in vivo in xenograft animals. Collectively, UA diminishes the proliferation and metastasis of gastric cancer via the regulation of Hippo pathway through Rassf1, which suggests that UA can be used as a potential chemopreventive and therapeutic agent for gastric cancer.

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