Evidence map›Paper›PMID 12717839›Full record

ArticleWorld journal of gastroenterology2003

Tumor necrosis factor-related apoptosis-inducing ligand gene on human colorectal cancer cell line HT29.

Xiang-Ming Xu, Chao He, Xiao-Tong Hu, Bing-Liang Fang

Abstract read
In one paragraph

Article in World journal of gastroenterology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Xiang-Ming XuDepartment of Colorectal Surgery of the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.
Chao He
Xiao-Tong Hu
Bing-Liang Fang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo evaluate the therapeutic efficiency of Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) gene on human colorectal cancer cell line HT29.

methodsHuman embryonal kidney cells transformed by introducing sheared fragments of Ad5 DNA (293 cell) were used for amplification of adenoviral vectors: Ad/GT-TRAIL,Ad/GT-Bax, Ad/GT-LacZ and Ad/PGK-GV16. Human colorectal cancer cell line HT29 was transfected with binary adenovirus-mediated TRAIL gene. Bax gene was used as positive control, LacZ gene was used as the vector control,and cells treated with PBS only were used as a mock control. The morphological changes, cell growth and apoptosis were measured by reversmicroscope, MTT method and flow cytometry.

resultsAll adenoviral vectors titer determined by optical absorbency at A260nm were 1X10(10) viral particle/ml(vp/ml). Obviously morphological changes of HT29 cells were observed when infected with Ad/GT-TRAIL, and these changes were much more obviously when Ad/PGK-GV16 was coinfected. The cell suppression percentage and the percentage of apoptotic cells were 52.5 % and 16.5 % respectively when infected with Ad/GT-TRAIL alone, while combining with Ad/PGK-GV16, the growth of HT29 was suppressed by 85.2 % and the percentage of apoptotic cells was 35.9 %. It showed a significantly enhanced therapeutic efficiency with binary system (P<0.05).

conclusionA binary adenoviral vector system provides an effective approach to amplify viral vectors that express potentially toxic gene, TRAIL. Ad/GT-TRAIL showed a significantly enhanced therapeutic efficiency for HT29 when coinfected with Ad/PGK-GV16. Ad/GT-TRAIL could induce apoptosis of HT29 and inhibit its growth.

Indexed as

AdenoviridaeApoptosisApoptosis Regulatory ProteinsCell DivisionCell SurvivalColorectal NeoplasmsGenetic TherapyGenetic VectorsHumansMembrane GlycoproteinsTNF-Related Apoptosis-Inducing LigandTransfectionTumor Cells, CulturedTumor Necrosis Factor-alphaApoptosis Regulatory ProteinsMembrane GlycoproteinsTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID12717839
PMCPMC4611406

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.