Evidence map›Paper›PMID 30662679›Full record

ArticleAmerican journal of translational research2018

Tuft1 promotes thyroid carcinoma cell invasion and proliferation and suppresses apoptosis through the Akt-mTOR/GSK3β signaling pathway.

Huifang Liu, Jing Zhu, Ziming Mao, Guangya Zhang, Xi Hu, Fengling Chen

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  4. Review
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  7. Review
  8. Morphological and Molecular Responses ofInternational journal of molecular sciences · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. [Expression of tuftelin protein and its clinical value in HBV-related liver cancer tissues].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021
    Article
  14. Tuftelin and HIFs expression in osteogenesis.Histochemistry and cell biology · 2019
    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

6 authors at 1 institution in 1 country.

Huifang LiuDepartment of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 201999, China.
Jing ZhuDepartment of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 201999, China.
Ziming MaoDepartment of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 201999, China.
Guangya ZhangDepartment of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 201999, China.
Xi HuDepartment of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 201999, China.
Fengling ChenDepartment of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 201999, China.
Shanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we aimed to investigate the biological functions of Tuftelin 1 (Tuft1) in thyroid carcinoma (TC) and determine its underlying molecular mechanism. We found that the expression of Tuft1 was significantly upregulated in TC tissues. Using TC tissue microarrays (n = 154), we found that Tuft1 expression was closely related with the overall survival (OS) and disease-free survival (DFS) of TC patients. Knockdown of Tuft1 in TPC-1 and SW579 cells suppressed the invasion and proliferation of TC cells and increased the apoptosis of TC cells. In vivo, knockdown of Tuft1 attenuated tumor growth and suppressed the phosphorylation of Akt, mTOR, and GSK3β signaling. Addition of recombinant Tuft1 protein (rTuft1) to TC cells increased the phosphorylation of Akt, mTOR, and GSK3β signaling. An mTOR inhibitor (Dactolisib) abrogated rTuft1 protein-induced TC cell invasion, proliferation, and apoptosis inhibition, whereas a GSK3β inhibitor (CHIR-98014) only abrogated rTuft1 protein-induced proliferation and apoptosis inhibition. These results suggest that Tuft1 promotes TC cell invasion and proliferation, and suppresses apoptosis through the Akt-mTOR or Akt-GSK3β signaling pathway. In the future, Tuft1 may serve as a potential therapeutic target for TC.

Indexed as

Akt-mTOR/GSK3βapoptosisinvasionproliferationthyroid carcinomaTuft1

Identifiers

PMID30662679
PMCPMC6325505
OpenAlexW2990653011

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.