Evidence map›Paper›PMID 28397069›Full record

ArticleNeurochemical research2017

LiCl Treatment Induces Programmed Cell Death of Schwannoma Cells through AKT- and MTOR-Mediated Necroptosis.

Ying Wang, Qi Zhang, Bo Wang, Peng Li, Pinan Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 23% 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, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Exploring treatment options in cancer: Tumor treatment strategies.Signal transduction and targeted therapy · 2024
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Rg1 Protects Hematopoietic Stem Cells from LiCl-Induced Oxidative Stress via Wnt Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  12. A Review of Drug Therapy in Vestibular Schwannoma.Drug design, development and therapy · 2021
    Review
  13. Review
  14. Review
  15. Improved detection of synthetic lethal interactions inProceedings of the National Academy of Sciences of the United States of America · 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

5 authors at 2 institutions in 1 country.

Ying WangBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Qi ZhangBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Bo WangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Peng LiDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Pinan LiuBeijing Neurosurgical Institute, Capital Medical University, Beijing, China. liupinan@yeah.net.
Capital Medical University · CNBeijing Tian Tan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lithium is considered a first-line therapy for the treatment of bipolar disorder and was recently shown to be associated with a reduced overall cancer risk. A growing body of evidence has indicated the potential antitumor benefits of this drug. Lithium likely functions as an antitumor agent. In this study, we found that lithium chloride (LiCl) significantly inhibits the proliferation of both RT4 cells and human NF2-associated primary schwannoma cells by inhibiting the expression of apoptosis-related proteins. LiCl-induced cell death exhibits ultrastructural features of necrosis and is reversed by the RIPK1-specific inhibitor necrostatin-1 in a dose-dependent manner, indicating that LiCl induces the necroptosis type of cell death. Moreover, LiCl treatment induces ROS generation and activates the AKT/mTOR pathway, which is reversed by necrostatin-1 treatment. Based on our results, LiCl treatment may induce the programmed cell death of schwannoma cells through AKT- and mTOR-mediated necroptosis, potentially representing a new mechanism by which LiCl induces tumor cell death. Moreover, LiCl may prove to be a new drug for treating schwannoma.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell DeathCell Line, TumorCell SurvivalDose-Response Relationship, DrugHumansLithium ChlorideNecrosisNeurilemmomaNeurofibromatosis 2Proto-Oncogene Proteins c-aktRatsTOR Serine-Threonine KinasesAntineoplastic AgentsLithium ChlorideMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKTLiClmTORNecroptosisNF2Schwannoma

Identifiers

PMID28397069
OpenAlexW2606577014

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.