Evidence map›Paper›PMID 29271385›Full record

ArticleChinese medical journal2018

Anti-apoptosis Effect of Decoy Receptor 3 in Cholangiocarcinoma Cell Line TFK-1.

Ying-Chen Xu, Jing Cui, Li-Jun Zhang, Dong-Xin Zhang, Bing-Chen Xing, Xiong-Wei-Ye Huang, Ji-Xiang Wu, Chao-Jie Liang, Guang-Ming Li

Open access · goldAbstract read
In one paragraph

Article in Chinese medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
0.1field-weighted citation impact, top 54% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 2 citations in OpenAlex.

  1. Molecular Targets and Signaling Pathways in Cholangiocarcinoma: A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2023
    Pooled it
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

9 authors at 2 institutions in 1 country.

Ying-Chen XuDepartment of Hepatobiliary Surgery, Surgical Laboratory, Beijing Tong Ren Hospital, Capital Medical University, Beijing 100730, China.
Jing CuiDepartment of Pathology, Capital Medical University, Beijing 100069, China.
Li-Jun ZhangDepartment of Hepatobiliary Surgery, Surgical Laboratory, Beijing Tong Ren Hospital, Capital Medical University, Beijing 100730, China.
Dong-Xin ZhangDepartment of Hepatobiliary Surgery, Surgical Laboratory, Beijing Tong Ren Hospital, Capital Medical University, Beijing 100730, China.
Bing-Chen XingDepartment of Hepatobiliary Surgery, Surgical Laboratory, Beijing Tong Ren Hospital, Capital Medical University, Beijing 100730, China.
Xiong-Wei-Ye HuangDepartment of Pathology, Capital Medical University, Beijing 100069, China.
Ji-Xiang WuDepartment of Hepatobiliary Surgery, Surgical Laboratory, Beijing Tong Ren Hospital, Capital Medical University, Beijing 100730, China.
Chao-Jie LiangDepartment of Hepatobiliary Surgery, Surgical Laboratory, Beijing Tong Ren Hospital, Capital Medical University, Beijing 100730, China.
Guang-Ming LiDepartment of Hepatobiliary Surgery, Surgical Laboratory, Beijing Tong Ren Hospital, Capital Medical University, Beijing 100730, China.
Capital Medical University · CNBeijing Tongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDecoy receptor 3 (DcR3) is a protein with anti-apoptotic effect that belongs to the tumor necrosis factor receptor superfamily. DcR3 is highly expressed in a variety of malignant tumors including cholangiocarcinoma and its expression was found to be related to the clinical stage, the invasion, and the metastasis of the tumor. This in vitro study aimed to investigate the effect of downregulated expression of DcR3 on cell viability, cell apoptosis, and cell cycle in cholangiocarcinoma cell line TFK-1.

methodsThree different cell lines were cultured: human cholangiocarcinoma TFK-1, human biliary epithelial carcinoma HuCCT-1, and human cholangiocarcinoma RBE. The cholangiocarcinoma cell line with the highest expression of DcR3 was selected for further investigation. The expression of DcR3 was silenced/knocked down by transfection with DcR3-siRNA in the selected cell line. Various biological phenotype parameters such as cell viability, apoptosis, and cell cycle were observed.

resultsThe mRNA and protein levels of DcR3 were measured in the three cell lines, and TFK-1 was selected. After the treatment with DcR3-siRNA for 48 h, DcR3 mRNA and protein expression in the treatment group were 38.45% (P < 0.01) and 48.03% (P < 0.05) of that of the control, respectively. It was found that the cell viability decreased to 61.87% of the control group (P < 0.01) after the downregulation of DcR3 in cholangiocarcinoma cell line TFK-1 by transfection with DcR3-siRNA, while the percentage of apoptotic cells was 2.98 times as compared with the control group (P < 0.05). Compared with the control group the ratio of G0/G1increased, and the ratio of G2/M decreased in the treatment group. However, the differences were not statistically significant.

conclusionsThe effect of DcR3 on the growth and apoptosis of cholangiocarcinoma has been demonstrated. DcR3 is not only a predictive marker for malignant tumor but it is also likely to be a potential target for cancer gene therapy. Further studies should focus on exploring the binding ligand of DcR3, the signaling pathway involved, and the molecular mechanism for the regulation of DcR3 expression in cholangiocarcinoma.

Indexed as

ApoptosisBile Duct NeoplasmsCell CycleCell DivisionCell Line, TumorCell SurvivalCholangiocarcinomaDown-RegulationGene Knockdown TechniquesHumansReceptors, Tumor Necrosis Factor, Member 6bRNA, Small InterferingSignal TransductionReceptors, Tumor Necrosis Factor, Member 6bRNA, Small Interfering

Identifiers

PMID29271385
PMCPMC5754963
OpenAlexW2782446118

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.