Regulation of MLH1 mRNA and protein expression by promoter methylation in primary colorectal cancer: a descriptive and prognostic cancer marker study

2013 ◽  
Vol 36 (5) ◽  
pp. 411-419 ◽  
Author(s):  
Lars Henrik Jensen ◽  
Anders Aamann Rasmussen ◽  
Lene Byriel ◽  
Hidekazu Kuramochi ◽  
Dorthe Gylling Crüger ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Protein Expression ◽  
Promoter Methylation ◽  
Primary Colorectal Cancer ◽  
Cancer Marker ◽  
Mrna And Protein Expression ◽  
Marker Study

Development of methodology to aid participation in colorectal cancer marker study

1984 ◽  
Vol 5 (3) ◽  
pp. 309
Author(s):  
Christina A. Lennon ◽  
Michael Baum ◽  
Joan Houghton ◽  
John Northover ◽  
Ian Saunders
Keyword(s):  
Colorectal Cancer ◽  
Cancer Marker ◽  
Marker Study

scholarly journals Noxa in colorectal cancer: a study on DNA, mRNA and protein expression

Oncogene ◽  
2003 ◽  
Vol 22 (30) ◽  
pp. 4675-4678 ◽  
Author(s):  
Agneta K Jansson ◽  
Anna M Emterling ◽  
Gunnar Arbman ◽  
Xiao-Feng Sun
Keyword(s):  
Colorectal Cancer ◽  
Protein Expression ◽  
Mrna And Protein Expression

scholarly journals ABCG2 expression, function, and promoter methylation in human multiple myeloma

Blood ◽  
2006 ◽  
Vol 108 (12) ◽  
pp. 3881-3889 ◽  
Author(s):  
Joel G. Turner ◽  
Jana L. Gump ◽  
Chunchun Zhang ◽  
James M. Cook ◽  
Douglas Marchion ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Flow Cytometry ◽  
Drug Resistance ◽  
Protein Expression ◽  
Cell Lines ◽  
Promoter Methylation ◽  
Plasma Cells ◽  
Cancer Resistance ◽  
Response To Chemotherapy ◽  
Mrna And Protein Expression

AbstractWe investigated the role of the breast cancer resistance protein (BCRP/ABCG2) in drug resistance in multiple myeloma (MM). Human MM cell lines, and MM patient plasma cells isolated from bone marrow, were evaluated for ABCG2 mRNA expression by quantitative polymerase chain reaction (PCR) and ABCG2 protein, by Western blot analysis, immunofluorescence microscopy, and flow cytometry. ABCG2 function was determined by measuring topotecan and doxorubicin efflux using flow cytometry, in the presence and absence of the specific ABCG2 inhibitor, tryprostatin A. The methylation of the ABCG2 promoter was determined using bisulfite sequencing. We found that ABCG2 expression in myeloma cell lines increased after exposure to topotecan and doxorubicin, and was greater in logphase cells when compared with quiescent cells. Myeloma patients treated with topotecan had an increase in ABCG2 mRNA and protein expression after treatment with topotecan, and at relapse. Expression of ABCG2 is regulated, at least in part, by promoter methylation both in cell lines and in patient plasma cells. Demethylation of the promoter increased ABCG2 mRNA and protein expression. These findings suggest that ABCG2 is expressed and functional in human myeloma cells, regulated by promoter methylation, affected by cell density, up-regulated in response to chemotherapy, and may contribute to intrinsic drug resistance.

scholarly journals Effects of PKM2 Gene Silencing on the Proliferation and Apoptosis of Colorectal Cancer LS-147T and SW620 Cells

2017 ◽  
Vol 42 (5) ◽  
pp. 1769-1778 ◽  
Author(s):  
Ran Ao ◽  
Lin Guan ◽  
Ying Wang ◽  
Jia-Ni Wang
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Gene Silencing ◽  
Cell Counting ◽  
Qrt Pcr ◽  
Empty Plasmid ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression ◽  
Sw620 Cells

Background/Aims: This paper aims to explore the effects of pyruvate kinase (PK) M2 gene silencing on the proliferation and apoptosis of colorectal cancer (CRC) LS-147T and SW620 cells. Methods: CRC LS-147T and SW620 cells highly expressing PKM2 were randomly selected by quantitative real-time polymerase chain reaction (qRT-PCR) and then assigned into the blank (no transfection), PKM2-shRNA (transfection with shRNA) and empty plasmid (transfection with empty plasmid) groups. Immunofluorescence was applied to detect PKM2 protein expression. qRT-PCR and Western blotting were conducted to assess mRNA and protein expression of PKM2, p53 and p21. The cell counting kit-8 (CCK-8) assay was used to assess cell proliferation. Flow cytometry was used to assess the cell cycle and apoptosis rate, and a senescence-associated β-galactosidase staining kit was used to assess cell senescence. Results: PKM2 exhibited high mRNA expression among CRC LS-147T and SW620 cells with remarkable protein expression noted in the cytoplasm and nucleus. The PKM2-shRNA group exhibited reduced PKM2 mRNA and protein expression, whereas p53 and p21 expression was increased compared with the blank and empty plasmid groups. Cell proliferation in PKM2-shRNA cells decreased significantly compared with the blank group and empty plasmid groups. The PKM2-shRNA group exhibited more cells in the G1 phase and fewer cells in the G2/M phase compared with the blank and empty plasmid groups. In addition, the PKM2-shRNA group exhibited significantly increased apoptosis rates and β-galactosidase activity compared with the blank and empty plasmid groups. Conclusion: Our study demonstrates that PKM2 gene silencing suppresses proliferation and promotes apoptosis in LS-147T and SW620 cells.

scholarly journals An aging and p53 related marker: HOXA5 promoter methylation negatively correlates with mRNA and protein expression in old age

Aging ◽  
2021 ◽  
Author(s):  
Laura-Kim Feiner ◽  
Sascha Tierling ◽  
Sebastian Holländer ◽  
Matthias Glanemann ◽  
Claudia Rubie
Keyword(s):  
Protein Expression ◽  
Old Age ◽  
Promoter Methylation ◽  
Mrna And Protein Expression

Topoisomerase I protein expression in primary colorectal cancer and recurrences after 5-FU-based adjuvant chemotherapy

2007 ◽  
Vol 133 (12) ◽  
pp. 1011-1015 ◽  
Author(s):  
P. Gouveris ◽  
A. C. Lazaris ◽  
T. G. Papathomas ◽  
A. Nonni ◽  
V. Kyriakou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Adjuvant Chemotherapy ◽  
Protein Expression ◽  
Topoisomerase I ◽  
Primary Colorectal Cancer

scholarly journals Phytic acid improves intestinal mucosal barrier damage and reduces serum levels of proinflammatory cytokines in a 1,2-dimethylhydrazine-induced rat colorectal cancer model

2018 ◽  
Vol 120 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Cuiping Liu ◽  
Chen Chen ◽  
Fuguo Yang ◽  
Xin Li ◽  
Lixue Cheng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Protein Expression ◽  
Phytic Acid ◽  
Proinflammatory Cytokines ◽  
Dose Group ◽  
Serum Levels ◽  
Mucosal Barrier ◽  
Intestinal Mucosal Barrier ◽  
Mrna And Protein Expression ◽  
E Cadherin

AbstractPhytic acid (PA) has been demonstrated to have a potent anticarcinogenic activity against colorectal cancer (CRC). Defects of the intestinal mucosal barrier and inflammation processes are involved in the development and progression of CRC. In the present study, we evaluated the effect of PA on the intestinal mucosal barrier and proinflammatory cytokines. After a 1-week acclimatisation period, sixty Wistar male rats were divided into the following five groups, with twelve rats per group: the control group (CG), model group (MG), low-PA-dose group (0·25 g/kg per d), middle-PA-dose group (0·5 g/kg per d), and high-PA-dose group (1 g/kg per d). 1,2-Dimethylhydrazine (DMH) at a dosage of 30 mg/kg of body weight was injected weekly to induce CRC for 18 weeks. We examined the expression of genes related to the intestinal mucosal barrier in the model. The results demonstrated that tumour incidence was decreased following PA treatment. The mRNA and protein expression of mucin 2 (MUC2), trefoil factor 3 (TFF3) and E-cadherin in the MG were significantly lower than those in the CG (P<0·05). The mRNA and protein expression of claudin-1 in the MG were significantly higher than those in the CG (P<0·05). PA elevated the mRNA and protein expression of MUC2, TFF3 and E-cadherin, and diminished the mRNA and protein expression of claudin-1. Furthermore, PA decreased serum levels of proinflammatory cytokines, which included TNF-α, IL-1β and IL-6. In conclusion, this study suggests that PA has favourable effects on the intestinal mucosal barrier and may reduce serum proinflammatory cytokine levels.

Sign in / Sign up

Export Citation Format

Share Document