Evidence map›Paper›PMID 35850753›Full record

ArticleBMC cancer2022

TTK Protein Kinase promotes temozolomide resistance through inducing autophagy in glioblastoma.

Jian Yu, Ge Gao, Xiangpin Wei, Yang Wang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Small Molecule Tyrosine Kinase Inhibitors (TKIs) for Glioblastoma Treatment.International journal of molecular sciences · 2024
    Review
  10. Article
  11. [Progress in the Study of Spindle Assembly Checkpoint in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
    Article
  12. 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

4 authors at 1 institution in 1 country.

Jian YuDepartment of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, 17 Lujiang Road, Hefei, 230001, Anhui, China.
Ge GaoDepartment of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, 17 Lujiang Road, Hefei, 230001, Anhui, China.
Xiangpin WeiDepartment of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, 17 Lujiang Road, Hefei, 230001, Anhui, China.
Yang WangDepartment of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, 17 Lujiang Road, Hefei, 230001, Anhui, China. ahwy_neurosurgery@fsyy.ustc.edu.cn.
University of Science and Technology of China · CN

Funding

Natural Science Foundation of Anhui Province 1708085QH174
6 · The paper itself

Abstract

backgroundTemozolomide (TMZ) resistance remains the main therapy challenge in patients with glioblastoma multiforme (GBM). TTK Protein Kinase (TTK) contributes to the radioresistance and chemoresistance in many malignancies. However, the role of TTK in the TMZ resistance of GBM cells remains unknown.

methodsThe expression of TTK was measured by western blot. The proliferation of GBM cells was assessed through MTT assay and clonogenic assay. Cell apoptosis was evaluated using western blot. LC3B puncta were detected using immunohistochemistry staining. The mouse xenograft model was used to investigate the role of TTK in vivo.

resultsKnockdown of TTK increased the sensitivity of GBM cells to TMZ treatment, while overexpression of TTK induced TMZ resistance. Two specific TTK inhibitors, BAY-1217389 and CFI-402257, significantly inhibited GBM cell proliferation and improved the growth-suppressive effect of TMZ. In addition, the knockdown of TTK decreased the autophagy levels of GBM cells. Inhibition of TTK using specific inhibitors could also suppress the autophagy process. Blocking autophagy using chloroquine (CQ) abolished the TMZ resistance function of TTK in GBM cells and in the mouse model.

conclusionsWe demonstrated that TTK promotes the TMZ resistance of GBM cells by inducing autophagy in vitro and in vivo. The use of a TTK inhibitor in combination with TMZ might help to overcome TMZ resistance and improve therapy efficiency in GBM.

Indexed as

Brain NeoplasmsGlioblastomaAnimalsAntineoplastic Agents, AlkylatingAutophagyCell Cycle ProteinsCell Line, TumorDrug Resistance, NeoplasmExtracellular Signal-Regulated MAP KinasesHumansMiceProtein Serine-Threonine KinasesProtein-Tyrosine KinasesTemozolomideXenograft Model Antitumor AssaysAntineoplastic Agents, AlkylatingCell Cycle ProteinsExtracellular Signal-Regulated MAP KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesTemozolomideTTK protein, humanAutophagyGlioblastomaResistanceTemozolomideTTK

Identifiers

PMID35850753
PMCPMC9290216
OpenAlexW4285731415

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.