scholarly journals Adenovirus mediated p53 tumour suppressor gene therapy for human gastric cancer cells in vitro and in vivo

Gut ◽  
1999 ◽  
Vol 44 (3) ◽  
pp. 366-371 ◽  
Author(s):  
M Ohashi ◽  
F Kanai ◽  
H Ueno ◽  
T Tanaka ◽  
K Tateishi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gene Therapy ◽  
P53 Gene ◽  
Human Gastric Cancer ◽  
Wild Type ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Wild Type P53

BACKGROUND/AIMSGastric cancer is one of the most prevalent forms of cancer in East Asia. Point mutation of the p53 gene has been reported in more than 60% of cases of gastric cancer and can lead to genetic instability and uncontrolled cell proliferation. The purpose of this investigation was to evaluate the potential of p53 gene therapy for gastric cancer.METHODSThe responses of human gastric cancer cell lines, MKN1, MKN7, MKN28, MKN45, and TMK-1, to recombinant adenoviruses encoding wild type p53 (AdCAp53) were analysed in vitro. The efficacy of the AdCAp53 treatment for MKN1 and MKN45 subcutaneous tumours in nude mice was assessed in vivo.RESULTSp53-specific growth inhibition was observed in vitro in two of four gastric cancer cell lines with mutated p53, but not in the wild type p53 cell line. The mechanism of the killing of gastric cancer cells by AdCAp53 was found, by flow cytometric analysis and detection of DNA fragmentation, to be apoptosis. In vivo studies showed that the growth of subcutaneous tumours of p53 mutant MKN1 cells was significantly inhibited by direct injection of AdCAp53, but no significant growth inhibition was detected in the growth of p53 wild type MKN45 tumours.CONCLUSIONSAdenovirus mediated reintroduction of wild type p53 is a potential clinical utility in gene therapy for gastric cancers.

Murine Double Minute 2 siRNA and wild-type p53 gene therapy interact positively with zinc on prostate tumours in vitro and in vivo

2014 ◽  
Vol 50 (6) ◽  
pp. 1184-1194 ◽  
Author(s):  
Junlian Gu ◽  
Bo Wang ◽  
Yanan Liu ◽  
Lingzhi Zhong ◽  
Yufeng Tang ◽  
...  
Keyword(s):  
Gene Therapy ◽  
P53 Gene ◽  
Wild Type ◽  
Double Minute ◽  
Murine Double Minute ◽  
Wild Type P53

scholarly journals LncRNA UCA1 promotes development of gastric cancer via the miR-145/MYO6 axis

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
An Yang ◽  
Xin Liu ◽  
Ping Liu ◽  
Yunzhang Feng ◽  
Hongbo Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Development Of Gastric Cancer

Abstract Background Long noncoding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1) is aberrantly expressed in multiple cancers and has been verified as an oncogene. However, the underlying mechanism of UCA1 in the development of gastric cancer is not fully understood. In the present study, we aimed to identify how UCA1 promotes gastric cancer development. Methods The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to analyze UCA1 and myosin VI (MYO6) expression in gastric cancer. Western blot and quantitative real-time PCR (QPCR) were performed to test the expression level of the UCA1/miR-145/MYO6 axis in gastric cancer cell lines and tissues. The roles of the UCA1/miR-145/MYO6 axis in gastric cancer in vitro and in vivo were investigated by CCK-8 assay, flow cytometry, siRNAs, immunohistochemistry, and a mouse xenograft model. The targeted relationship among UCA1, miR-145, and MYO6 was predicted using LncBase Predicted v.2 and TargetScan online software, and then verified by luciferase activity assay and RNA immunoprecipitation. Results UCA1 expression was higher but miR-145 expression was lower in gastric cancer cell lines or tissues, compared to the adjacent normal cell line or normal tissues. Function analysis verified that UCA1 promoted cell proliferation and inhibited cell apoptosis in the gastric cancer cells in vitro and in vivo. Mechanistically, UCA1 could bind directly to miR-145, and MYO6 was found to be a downstream target gene of miR-145. miR-145 mimics or MYO6 siRNAs could partly reverse the effect of UCA1 on gastric cancer cells. Conclusions UCA1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-145 to upregulate MYO6 expression in gastric cancer, indicating that the UCA1/miR-145/MYO6 axis may serve as a potential therapeutic target for gastric cancer.

Oleanolic acid induces autophagic death in human gastric cancer cells in vitro and in vivo

2016 ◽  
Vol 40 (7) ◽  
pp. 770-778 ◽  
Author(s):  
Hao Nie ◽  
Yu Wang ◽  
Yong Qin ◽  
Xing-Guo Gong
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Oleanolic Acid ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

Wild Type p53 Gene Sensitizes Rat C6 Glioma Cells to HSV-TK/ACV Treatment In Vitro and In Vivo

2010 ◽  
Vol 16 (4) ◽  
pp. 509-514 ◽  
Author(s):  
Qiang Huang ◽  
Zhibo Xia ◽  
Yongping You ◽  
Peiyu Pu
Keyword(s):  
Glioma Cells ◽  
P53 Gene ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Wild Type ◽  
Wild Type P53 ◽  
Rat C6 Glioma

scholarly journals Wild-type p53 gene transfer is not detrimental to normal cells in vivo: implications for tumor gene therapy

Oncogene ◽  
2004 ◽  
Vol 23 (2) ◽  
pp. 418-425 ◽  
Author(s):  
Gianluca Bossi ◽  
Giuseppina Mazzaro ◽  
Alessandro Porrello ◽  
Marco Crescenzi ◽  
Silvia Soddu ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Gene Transfer ◽  
P53 Gene ◽  
Wild Type ◽  
Normal Cells ◽  
Tumor Gene Therapy ◽  
Wild Type P53 ◽  
Tumor Gene

scholarly journals Silencing of TKTL1 by siRNA inhibits proliferation of human gastric cancer cells in vitro and in vivo

2010 ◽  
Vol 9 (9) ◽  
pp. 710-716 ◽  
Author(s):  
Weijie Yuan ◽  
Shaobin Wu ◽  
Jianwu Guo ◽  
Zhikang Chen ◽  
Jie Ge ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals Comprehensive Genomic Characterization Analysis Identifies an Oncogenic Pseudogene RP11-3543B.1 in Human Gastric Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Xin Chen ◽  
Zhenyao Chen ◽  
Hao Wu ◽  
Xianghua Liu ◽  
Fengqi Nie ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Expression Profiling ◽  
The Cancer Genome Atlas ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Altered Expression ◽  
Genomic Characterization

Background: Gastrointestinal Cancer (GICs) is the most common group of malignancies, and many of its types are the leading causes of cancer related death worldwide. Pseudogenes have been revealed to have critical regulatory roles in human cancers. The objective of this study is to comprehensive characterize the pseudogenes expression profiling and identify key pseudogenes in the development of gastric cancer (GC).Methods: The pseudogenes expression profiling was analyzed in six types of GICs cancer from The Cancer Genome Atlas RNA-seq data to identify GICs cancer related pseudogenes. Meanwhile, the genomic characterization including somatic alterations of pseudogenes was analyzed. Then, CCK8 and colony formation assays were performed to evaluate the biological function of RP11-3543B.1 and miR-145 in gastric cancer cells. The mechanisms of pseudogene RP11-3543B.1 in GC cells were explored via using bioinformatics analysis, next generation sequencing and lucifarese reporter assay.Results: We identified a great number of pseudogenes with significantly altered expression in GICs, and some of these pseudogenes expressed differently among the six cancer types. The amplification or deletion in the pseudogenes-containing loci involved in the alterations of pseudogenes expression in GICs. Among these altered pseudogenes, RP11-3543B.1 is significantly upregulated in gastric cancer. Down-regulation of RP11-3543B.1 expression impaired GC cells proliferation both in vitro and in vivo. RP11-3543B.1 exerts oncogene function via targeting miR-145-5p to regulate MAPK4 expression in gastric cancer cells.Conclusion: Our study reveals the potential of pseudogenes expression as a new paradigm for investigating GI cancer tumorigenesis and discovering prognostic biomarkers for patients.

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