Effects of nickel poisoning on expression pattern of the 72/73 and 94 kDa stress proteins in rat organs and in the COS-7, HepG2, and A549 cell lines

2005 ◽  
Vol 19 (1) ◽  
pp. 12-18 ◽  
Author(s):  
N. Hfaiedh ◽  
M. S. Allagui ◽  
A. El Feki ◽  
Y. Gaubin ◽  
J. C. Murat ◽  
...  
2006 ◽  
Vol 44 (7) ◽  
pp. 1031-1037 ◽  
Author(s):  
A. Soussi ◽  
Y. Gaubin ◽  
B. Beau ◽  
J.C. Murat ◽  
J.P. Soleilhavoup ◽  
...  

Author(s):  
Mojgan Azadpour ◽  
Mohammad Mehdi Farajollahi ◽  
Ali Mohammad Varzi ◽  
Pejman Hashemzadeh ◽  
Hossein Mahmoudvand ◽  
...  

Introduction: This study aimed to evaluate the antioxidant property of silymarin (SM) extracted from the seed of Silybum marianum and its anticancer activity on KB and A549 cell lines following 24, 48, and 72 h of treatment. Methods: Ten grams of powdered S. marianum seeds were defatted using n-hexane for 6 hours and then extracted by methanol. The silymarin extracted of extraction components The extracted components of silymarin were measured by spectrophotometric assay and HPLC analysis. 2, 2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging, phenol content, total flavonoid content, and total antioxidant capacity were measured to detect the antioxidant properties of SM. The anticancer activity of the SM on cell lines evaluated by MTT. Results: In HPLC analysis, more than 50% of the peaks were related to silibin A and B. SM was reducedDPPH (the stable free radical) with a 50% inhibitory concentration (IC50) of 6.56 μg/ ml in comparison with butylated hydroxyl toluene (BHT), which indicated an IC50 of ~3.9 μg/ ml.The cytotoxicity effect of SM on the cell lines was studied by MTT assay. The cytotoxicity effect of the extracted silymarin on KB and A549 cell lines was observed up to 80 and 70% at 156 and 78 µg/ml, respectively. The IC50 value of the extracted SM on KB and A549 cell lines after 24 hours of treatment was seen at 555 and 511 µg/ml, respectively. Conclusion: Due to the good antioxidant and anticancer properties of the isolated silymarin, its use as an anticancer drug is suggested.


2021 ◽  
Vol 11 ◽  
Author(s):  
Huili Li ◽  
Jiliang Wang ◽  
Kun Huang ◽  
Tao Zhang ◽  
Lu Gao ◽  
...  

NK2 homeobox 5 (Nkx2.5), a homeobox-containing transcription factor, is associated with a spectrum of congenital heart diseases. Recently, Nkx2.5 was also found to be differentially expressed in several kinds of tumors. In colorectal cancer (CRC) tissue and cells, hypermethylation of Nkx2.5 was observed. However, the roles of Nkx2.5 in CRC cells have not been fully elucidated. In the present study, we assessed the relationship between Nkx2.5 and CRC by analyzing the expression pattern of Nkx2.5 in CRC samples and the adjacent normal colonic mucosa (NCM) samples, as well as in CRC cell lines. We found higher expression of Nkx2.5 in CRC compared with NCM samples. CRC cell lines with poorer differentiation also had higher expression of Nkx2.5. Although this expression pattern makes Nkx2.5 seem like an oncogene, in vitro and in vivo tumor suppressive effects of Nkx2.5 were detected in HCT116 cells by establishing Nkx2.5-overexpressed CRC cells. However, Nkx2.5 overexpression was incapacitated in SW480 cells. To further assess the mechanism, different expression levels and mutational status of p53 were observed in HCT116 and SW480 cells. The expression of p21WAF1/CIP1, a downstream antitumor effector of p53, in CRC cells depends on both expression level and mutational status of p53. Overexpressed Nkx2.5 could elevate the expression of p21WAF1/CIP1 only in CRC cells with wild-type p53 (HCT116), rather than in CRC cells with mutated p53 (SW480). Mechanistically, Nkx2.5 could interact with p53 and increase the transcription of p21WAF1/CIP1 without affecting the expression of p53. In conclusion, our findings demonstrate that Nkx2.5 could act as a conditional tumor suppressor gene in CRC cells with respect to the mutational status of p53. The tumor suppressive effect of Nkx2.5 could be mediated by its role as a transcriptional coactivator in wild-type p53-mediated p21WAF1/CIP1 expression.


2021 ◽  
Vol 11 (6) ◽  
pp. 103-115
Author(s):  
Benoite. T ◽  
Nora Vigasini K

Non-communicable diseases like diabetes and cancer are the major cause of death worldwide. Various drugs are used for the treatment of these diseases. However, they cause lots of side effects. There is a need for alternate drugs with fewer side effects. Medicinal plants serve as a good source for alternate form of treatment. Therefore, in this study, ethanolic and aqueous extracts of D. regia flowers were evaluated for their antioxidant, antidiabetic, anti-inflammatory and cytotoxic activity to justify its use as a medicinal plant. Total phenol and flavonoid content of the extracts were measured. GC-MS analysis of the extracts were done to investigate the presence of various bioactive compounds. Antioxidant activity was assessed by radical scavenging and reduction assays. Antidiabetic activity was assessed by the ability of extracts to inhibit enzyme alpha amylase. Anti-inflammatory activity was evaluated by membrane stabilization activity. Anticancer activity against MCF-7 and A549 cell lines were measured by the MTT assay.The ethanolic extract contained more phenols (282.940.80 mgGAE/g) and flavonoids (140.912.27 mgQE/g). GC-MS analysis showed the presence of compounds belonging to fatty acids, alkanes, phenols and organic alcohols. The aqueous extract showed strong superoxide radical scavenging activity with a low IC50 of 39.35±0.74 µg/mL. The ethanolic extract showed higher ferric reducing power with an IC50 of 59.65±0.28µg/mL. Ethanolic extract was more potent in inhibiting alpha amylase with a low IC50 value of 47.14±0.6 µg/mL. Ethanolic extract also showed maximum inhibition of 88.86±0.1% against heat induced lysis of cell membrane. Both extracts affected the proliferation of MCF-7 and A549 cell lines at 160 µg/mL. The results of the present study support the use of D. regia flower as a potential source of bioactive phytochemicals and can be used as a plant-based antioxidant, antidiabetic, anti-inflammatory and anticancer agent.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yue Luo ◽  
Junhao Lin ◽  
Jiakang Zhang ◽  
Zhenghui Song ◽  
Dayong Zheng ◽  
...  

Long noncoding RNAs (lncRNAs) have been substantially reported to have critical roles in regulating tumorigenesis in recent years. However, the expression pattern and biological function of SNHG17 in hepatocellular carcinoma (HCC) remain unclear. Bioinformatics analysis and qRT-PCR were performed to detect the expression pattern of SNHG17 in HCC tissues, adjacent nontumorous tissues, and cell lines. The effect of SNHG17 on proliferation, migration, and apoptosis of HCC was investigated by knockdown and overexpressing SNHG17 in HCC cell lines. RNA sequencing was utilized to explore the underlying mechanism. Utilizing publicly available TCGA-LIHC, GSE102079 HCC datasets, and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion, and advanced TNM stage. Furthermore, gain- and loss-of-function studies demonstrated that SNHG17 promoted cell proliferation and migration and inhibited apoptosis of HCC. By employing RNA sequencing, we found knockdown of SNHG17 caused 1037 differentially expressed genes, highly enriched in several pathways, including metabolic, PI3K-Akt, cell adhesion, regulation of cell proliferation, and apoptotic pathway; among them, 92 were overlapped with SNHG17-related genes in the TCGA-LIHC dataset. Furthermore, ERH, TBCA, TDO2, and PDK4 were successfully validated and found significantly dysregulated in HCC tissues. Moreover, HCC patients with higher SNHG17 expression had a relatively poor overall survival and disease-free survival, and ERH and PDK4 also played a marked role in the prognosis of HCC. Broadly, our findings illustrate that SNHG17 acts as a noncoding oncogene in HCC progression, suggesting its potential value as a novel target for HCC therapy.


Author(s):  
Robert Nowakowski ◽  
Beniamin Grabarek ◽  
Anna Burnat-Olech ◽  
Dariusz Boroń ◽  
Monika Paul-Samojedny

Background: This study aimed to evaluate the variances in the expression pattern of mRNAs and miRNAs related to the EMT in the Ishikawa (histological grade 1; G1), EC-1A (histological grade 2; G2), and KLE (histological grade 3; G3) cell cultures under cisplatin treatment. Methods: Endometrial cancer cell lines were exposed to 75.22 mg (an average concentration of the drug used in patients with endometrial cancer) for 12.24 and 48 hours compared to the untreated cells (control). The molecular analysis included extraction of total RNA, microarray analysis (mRNA and miRNA), RTqPCR, and the ELISA assay. Results: Out of 226 mRNAs associated with the EMT, the number of mRNAs differentially expressed in endometrial cancer cell cultures treated with cisplatin compared to a control culture was as follows: Ishikawa line - 87 mRNAs; EC-1A - 84 mRNAs; KLE - 71 mRNAs (p<0.05). The greatest changes in the Ishikawa line treated with the drug compared to the control were noticed for mRNA STAT1 TGFβ1, SMAD3, FOXO8, whereas in EC-1A, they were mRNA TGFβ1, BAMBI, SMAD4, and in KLE mRNA COL1A1, FOXO8, TGFβ1. The analysis also showed that miR-106a, miR-30d, miR-300 are common for all cell lines used in this experiment. Conclusion: Cisplatin changes the expression profile of genes associated with EMT in endometrial cancer cell lines. It seems that the expression pattern of TGFβ1 might be a promising, supplementary molecular marker of the effectiveness of cisplatin therapy. The analysis showed that miR-30d, miR-300, and miR-106a are involved in the regulation of the expression of EMT-related genes.


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