Expression of Five Selected Human Mismatch Repair Genes Simultaneously Detected in Normal and Cancer Cell Lines by a Nonradioactive Multiplex Reverse Transcription-Polymerase Chain Reaction

Pathobiology ◽  
1997 ◽  
Vol 65 (6) ◽  
pp. 293-300 ◽  
Author(s):  
Qingyi Wei ◽  
Yongli Guan ◽  
Lie Cheng ◽  
Robert Radinsky ◽  
Menashe Bar-Eli ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Mismatch Repair ◽  
Cell Lines ◽  
Cancer Cell ◽  
Reverse Transcription ◽  
Cancer Cell Lines ◽  
Mismatch Repair Genes ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Repair Genes

Expression of prolactin and growth hormone receptor genes and their isoforms in the gastrointestinal tract

1995 ◽  
Vol 268 (3) ◽  
pp. G431-G442 ◽  
Author(s):  
M. Nagano ◽  
E. Chastre ◽  
A. Choquet ◽  
J. Bara ◽  
C. Gespach ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Hormone ◽  
Polymerase Chain Reaction ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Gi Tract ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Ht 29

Distribution of transcripts for prolactin and growth hormone receptors (PRLR and GHR) and their isoforms was characterized in the gastrointestinal (GI) tract from several species by reverse transcription-polymerase chain reaction combined with Southern analysis. Human, rabbit, and fetal and adult rat PRLR and GHR transcripts were detected in isolated gastric glands, gastric cell fractions, and intestinal mucosa lineages. Human PRLR and GHR transcripts were also observed throughout the cancerous progression of the colonic and gastric mucosa from adenomas to colonic liver metastasis and gastrointestinal cancer cell lines at various stages of growth and differentiation. Prolactin (PRL) produced no detectable effect on M1 gastric mucin secretion in HT-29 cells adapted to methotrexate (HT-29-MTX) or on acid secretion in isolated rabbit parietal cells. GHRd3, an isoform of human GHR transcript missing exon 3, was also broadly expressed and was the only form found in gastric and colorectal adenocarcinomas. Interestingly, several extra bands of polymerase chain reaction products of the human PRLR, which were smaller than the expected size, were observed not only in the GI tract but also in liver and T-47D breast cancer cells. These products from human intestinal and breast cancer cell lines were subsequently subcloned and sequenced, and we isolated six isoforms of the receptor transcripts. One of these clones encodes a putative human PRL binding protein. The expression of PRL and PRLR transcripts was also clearly observed in intraepithelial lymphocytes purified from the mouse intestine. The widespread expression of the PRL and GH receptor transcripts in gastric and intestinal mucosal lineages, particularly in epithelia, suggests regulatory roles of these hormones on digestive and immune functions, including metabolism, growth, or differentiation.

scholarly journals Expression of survivin in bladder cancer cell lines using quantitative real-time polymerase chain reaction

2014 ◽  
Vol 25 (1) ◽  
pp. 19-21 ◽  
Author(s):  
Kee-Thai Kiu ◽  
Thomas I.S. Hwang ◽  
Hsiao-Yen Hsieh ◽  
Cheng-Huang Shen ◽  
Yuan-Hung Wang ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Bladder Cancer ◽  
Real Time ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Bladder Cancer Cell ◽  
Chain Reaction ◽  
Polymerase Chain

Expression of DNA repair genes in oral squamous cell carcinoma using reverse transcription-quantitative polymerase chain reaction

2020 ◽  
Vol 130 (3) ◽  
pp. 298-305
Author(s):  
Mônica Ghislaine Oliveira Alves ◽  
Natália da Silva Miguel ◽  
Camila Cristina Panisello Ferreira ◽  
Elis Ribeiro Alvarenga ◽  
Bruna Manzanares Tonon ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Squamous Cell Carcinoma ◽  
Dna Repair ◽  
Oral Squamous Cell Carcinoma ◽  
Reverse Transcription ◽  
Quantitative Polymerase Chain Reaction ◽  
Dna Repair Genes ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Repair Genes

scholarly journals Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells

2019 ◽  
Vol 18 ◽  
pp. 153303381984254
Author(s):  
Nannan Ao ◽  
Yingchu Dai ◽  
Qianping Chen ◽  
Yang Feng ◽  
Jingping Yu ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Chain Reaction ◽  
Bortezomib Treatment ◽  
Esophageal Cancer Cell ◽  
Polymerase Chain ◽  
Human Esophageal Cancer ◽  
Microarray Chips

Objectives: Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways. Methods: Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction. Results: The proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G2/M arrest and apoptosis. Microarray chips revealed multiple signaling pathways targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt-, and calcium-mediated pathway. The expression patterns of 4 representative genes UBD, CUL3, HDAC6, and GADD45A were verified by quantitative real-time polymerase chain reaction and showed consistency with the microarray assay. Conclusion: Bortezomib could suppress cell viability, cause G2/M arrest, and induce apoptosis in human esophageal cancer cells, with possible targets including UBD, CUL3, HDAC6, and GADD45A.

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