Evidence map›Paper›PMID 27356491›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2016

Targeting Transforming Growth Factor-Beta1 (TGF-β1) Inhibits Tumorigenesis of Anaplastic Thyroid Carcinoma Cells Through ERK1/2-NFκkB-PUMA Signaling.

Qiang Yin, Shan Liu, Anbing Dong, Xiufang Mi, Fengyun Hao, Kejun Zhang

RetractedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Cell Component and Function of Tumor Microenvironment in Thyroid Cancer.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Article
  5. Review
  6. Acceleration of BRAFEndocrine · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Qiang YinDepartment of Oncology, People's Hospital of Rizhao, Rizhao, Shandong, China (mainland).
Shan LiuDepartment of Oncology, People's Hospital of Rizhao, Rizhao, Shandong, China (mainland).
Anbing DongDepartment of Thyroid Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Xiufang MiDepartment of Internal Medicine, People's Hospital of Zhangqiu, Jinan, Shandong, China (mainland).
Fengyun HaoDepartment of Pathology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Kejun ZhangDepartment of Thyroid Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Qingdao University · CNPeople’s Hospital of Rizhao · CNZhangqiu City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND The transforming growth factor-beta (TGF-β) signaling pathway plays a critical role in promoting tumor growth. TGF-β1was found to be overexpressed in anaplastic thyroid cancer (ATC). We therefore tested our hypothesis that targeting TGF-β1 inhibits tumorigenesis of ATC cells. MATERIAL AND METHODS Effects of TGF-β1 stimulation or TGF-β1 inhibition by small interfering RNA (TGF-β1siRNA) on proliferation, colony formation, and apoptosis in 8505C cells in vitro was detected using siRNAs and inhibitors to examine the TGF-β1 signaling pathway. A subcutaneously implanted tumor model of 8505C cells in nude mice was used to assess the effects of TGF-β1 inhibition on tumorigenesis development. RESULTS TGF-β1siRNAs decreased proliferation and colony formation, and increased apoptosis in 8505C cells in vitro and inhibited tumor growth in vivo. TGF-β1siRNA inhibited phosphorylation ERK1/2 (pERK1/2) and increased p65-dependant PUMA mRNA and protein expression. Knockdown of p65 or PUMA by siRNA reduced TGF-β1siRNA-induced apoptosis, as well as caspase-3 and PARP activation. Upregulation of p65 or PUMA expression by TGF-β1siRNA requires pERK1/2 inhibition. TGF-β1 shRNA inhibited tumor growth in vivo. CONCLUSIONS Therapies targeting the TGF-β1 pathway may be more effective to prevent primary tumor formation. The ability of this therapy to decrease tumorigenesis may be related to ERK1/2/NF-κB/PUMA signaling.

Indexed as

MAP Kinase Signaling SystemAnimalsApoptosisApoptosis Regulatory ProteinsCarcinogenesisCaspase 3Cell Line, TumorCell Transformation, NeoplasticFemaleHeterograftsHumansMiceMice, NudeNF-kappa BProto-Oncogene ProteinsRNA, Small InterferingApoptosis Regulatory ProteinsBBC3 protein, humanCaspase 3NF-kappa BProto-Oncogene ProteinsRNA, Small InterferingTransforming Growth Factor beta1

Identifiers

PMID27356491
PMCPMC4933554
OpenAlexW2465200210

What OpenQuestion holds

Textmetadata
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.