Evidence map›Paper›PMID 32742128›Full record

ArticleWorld journal of gastroenterology2020

TBL1XR1 induces cell proliferation and inhibit cell apoptosis by the PI3K/AKT pathway in pancreatic ductal adenocarcinoma.

Jian-Feng Gu, Wei Fu, Hai-Xin Qian, Wen-Xiu Gu, Yang Zong, Qian Chen, Long Lu

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Nuclear Receptors in Energy Metabolism.Advances in experimental medicine and biology · 2022
    Article
  8. Scoparone inhibits pancreatic cancer through PI3K/Akt signaling pathway.World journal of gastrointestinal oncology · 2021
    Article
  9. Article
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

7 authors at 1 institution in 1 country.

Jian-Feng GuDepartment of General Surgery, Changshu No. 1 People's Hospital Affiliated to Soochow University, Changshu 215500, Jiangsu Province, China. jscsgjf@sina.cn.
Wei FuDepartment of Oncology, Changshu No. 1 People's Hospital Affiliated to Soochow University, Changshu 215500, Jiangsu Province, China.
Hai-Xin QianDepartment of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China.
Wen-Xiu GuDepartment of General Surgery, Changshu No. 1 People's Hospital Affiliated to Soochow University, Changshu 215500, Jiangsu Province, China.
Yang ZongDepartment of General Surgery, Changshu No. 1 People's Hospital Affiliated to Soochow University, Changshu 215500, Jiangsu Province, China.
Qian ChenDepartment of General Surgery, Changshu No. 1 People's Hospital Affiliated to Soochow University, Changshu 215500, Jiangsu Province, China.
Long LuDepartment of Oncology, Changshu No. 1 People's Hospital Affiliated to Soochow University, Changshu 215500, Jiangsu Province, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is one of the deadliest solid tumors. Identification of diagnostic and therapeutic biomarkers for PDAC is urgently needed. Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) has been linked to the progression of various human cancers. Nevertheless, the function and role of TBL1XR1 in pancreatic cancers are unclear.

aimTo elucidate the function and potential mechanism of TBL1XR1 in the development of PDAC.

methodsNinety patients with histologically-confirmed PDAC were included in this study. PDAC tumor samples and cell lines were used to determine the expression of TBL1XR1. CCK-8 assays and colony formation assays were carried out to assess PDAC cell viability. Flow cytometry was performed to measure the changes in the cell cycle and cell apoptosis. Changes in related protein expression were measured by western blot analysis. Animal analysis was conducted to confirm the impact of TBL1XR1

resultsPatients with TBL1XR1-positive tumors had worse overall survival than those with TBL1XR1-negative tumors. Moreover, we found that TBL1XR1 strongly promoted PDAC cell proliferation and inhibited PDAC cell apoptosis. Moreover, knockdown of TBL1XR1 induced G0/G1 phase arrest.

conclusionTBL1XR1 promoted PDAC cell progression and might be an effective diagnostic and therapeutic marker for pancreatic cancer.

Indexed as

AdenocarcinomaCarcinoma, Pancreatic DuctalPancreatic NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Cytoplasmic and NuclearRepressor ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Cytoplasmic and NuclearRepressor ProteinsTBL1XR1 protein, humanPancreatic ductal adenocarcinomaPI3K/AKT pathwayProliferationTBL1XR1

Identifiers

PMID32742128
PMCPMC7366057
OpenAlexW3039133853

What OpenQuestion holds

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Registered trials

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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.