Evidence map›Paper›PMID 27447746›Full record

ArticleOncotarget2017

BTG1 might be employed as a biomarker for carcinogenesis and a target for gene therapy in colorectal cancers.

Shuang Zhao, Shu-Rui Chen, Xue-Feng Yang, Dao-Fu Shen, Yasuo Takano, Rong-Jian Su, Hua-Chuan Zheng

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. The p53 Pathway Related Genes Predict the Prognosis of Colon Cancer.International journal of general medicine · 2022
    Article
  6. The roles ofFrontiers in genetics · 2022
    Article
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  15. Overexpression and biological function of MEF2D in human pancreatic cancer.American journal of translational research · 2017
    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 2 institutions in 2 countries.

Shuang ZhaoCancer Center, Key Laboratory of Brain and Spinal Cord Injury of Liaoning Province, and Animal Center, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Shu-Rui ChenDepartment of Science and Technology, Jinzhou Medical University, Jinzhou, China.
Xue-Feng YangCancer Center, Key Laboratory of Brain and Spinal Cord Injury of Liaoning Province, and Animal Center, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Dao-Fu ShenCancer Center, Key Laboratory of Brain and Spinal Cord Injury of Liaoning Province, and Animal Center, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Yasuo TakanoSchool of Health Science, Tokyo University of Technology, Nishi-Kamata, Ohta-ku, Tokyo, Japan.
Rong-Jian SuLife Science Institute of Jinzhou Medical University, Jinzhou, China.
Hua-Chuan ZhengCancer Center, Key Laboratory of Brain and Spinal Cord Injury of Liaoning Province, and Animal Center, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Jinzhou Medical University · CNTokyo University of Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here, BTG1 overexpression inhibited proliferation, induced differentiation, autophagy, and apoptosis in colorectal cancer cells (p<0.05). BTG1 overexpression reduced mitochondrial membrane potential and caused senescence in HCT-116 transfectants (p<0.05). BTG1-induced G2 arrest might be related to Cyclin B1 and Cdc25B hypoexpression in HCT-15 transfectants, while G1 arrest in HCT-116 transfectants overexpressing p21 and p27. BTG1 overexpression decreased the expression of Bcl-2, Bcl-xL, XIAP, Akt1 or survivin and increased the expression of Bax or p53 in colorectal cancer cells. BTG1-induced autophagy was dependent on Beclin-1 expression. BTG1 overexpression might weaken β-catenin pathway in colorectal cancer cells. The chemosensitivity of BTG1 transfectants to paclitaxel, cisplatin, MG132 or SAHA was positively correlated with its apoptotic induction. There was a lower expression level of BTG1 in cancer than matched non-neoplastic mucosa by RT-PCR (p<0.05), while versa for Western blot and immunohistochemical data (p<0.05). BTG1 overexpression significantly suppressed the growth of HCT-15 and HCT-116 via inhibiting proliferation, inducing apoptosis and autophagy in nude mice. Up-regulated BTG1 expression plays an important role in colorectal carcinogenesis as a potential biomarker. BTG1 expression might reverse aggressive phenotypes, so it might be employed as a target of gene therapy for colorectal cancer.

Indexed as

AnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsAutophagybeta CateninCell Cycle ProteinsCell DifferentiationCell ProliferationColorectal NeoplasmsDose-Response Relationship, DrugFemaleG2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticGenetic TherapyHCT116 CellsAntineoplastic AgentsApoptosis Regulatory Proteinsbeta CateninBTG1 protein, humanCell Cycle ProteinsCTNNB1 protein, humanNeoplasm Proteinsp38 Mitogen-Activated Protein Kinasesaggressive phenotypesBTG1carcinogenesiscolorectal cancergene therapy

Identifiers

PMID27447746
PMCPMC5352338
OpenAlexW2490161305

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.