Evidence map›Paper›PMID 28260052›Full record

ArticleMolecular medicine reports2017

LMTK3 knockdown retards cell growth and invasion and promotes apoptosis in thyroid cancer.

Lu Lu, Xueli Yuan, Qiang Zhang, Hong Zhang, Baozhong Shen

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  6. Review
  7. The Inhibitory Properties of a Novel, Selective LMTK3 Kinase Inhibitor.International journal of molecular sciences · 2023
    Article
  8. Article
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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

5 authors at 3 institutions in 1 country.

Lu LuDepartment of Medical Oncology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Xueli YuanDepartment of Medical Oncology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Qiang ZhangCenter for Stem Cell and Translational Medicine, School of Life Sciences, Anhui University, Hefei, Anhui 230601, P.R. China.
Hong ZhangCenter for Stem Cell and Translational Medicine, School of Life Sciences, Anhui University, Hefei, Anhui 230601, P.R. China.
Baozhong ShenMolecular Imaging Center, Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Anhui University · CNHarbin Medical University · CNFourth Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lemur tyrosine kinase-3 (LMTK3) is a member of the serine/threonine tyrosine kinase family, which is thought to be involved in tumor progression and prognosis. The purpose of the present study was to determine the diagnostic significance and therapeutic targets in thyroid cancer. ELISA assay was used to detect the protein expression of serum LMTK3. Immunohistochemistry and reverse transcription‑quantitative polymerase chain reaction were employed to measure the expression of LMTK3. Flow cytometry was used to determine the cell cycle. Transwell assay was used to measure the invasion and migration of SW579 cells and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay to detect cell apoptosis. The LMTK3 level was positively associated with disease stage and pathological type, whereas there was no correlation between LMTK3 level and gender, age, tumor size or lymph node metastasis. The serum LMTK3 level was significantly increased in 102 thyroid carcinoma patients compared with 52 benign thyroid tumor patients and 50 healthy volunteers (P=0.001). The protein and mRNA expression of LMTK3 was markedly higher in thyroid cancer patients compared with patients with benign thyroid tumors. Notably, LMTK3 knockdown retarded proliferation, invasion and migration in SW579 cells. In addition, downregulation of LMTK3 promoted apoptosis in SW579 cells. These findings indicated that LMTK3 knockdown retards the growth of thyroid cancer cells partly through inhibiting proliferation, invasion, migration and inducing apoptosis in SW579 cells. It may serve as a useful diagnostic biomarker and a novel therapeutic target for patients with thyroid cancer.

Indexed as

Cell MovementCell ProliferationAdultAgedApoptosisCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMembrane ProteinsMiddle AgedNeoplasm InvasivenessProtein Serine-Threonine KinasesRNA, Small InterferingThyroid GlandLMTK3 protein, humanMembrane ProteinsProtein Serine-Threonine KinasesRNA, Small Interfering

Identifiers

PMID28260052
PMCPMC5364963
OpenAlexW2594194114

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.