Evidence map›Paper›PMID 33262323›Full record

ArticleSignal transduction and targeted therapy2020

MELK is an oncogenic kinase essential for metastasis, mitotic progression, and programmed death in lung carcinoma.

Qin Tang, Wan Li, Xiangjin Zheng, Liwen Ren, Jinyi Liu, Sha Li, Jinhua Wang, Guanhua Du

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

62 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Targeting PLK1 Reduces MMP10 to Enhance Radiosensitivity in HPV- Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. HighCancers · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Targeting MELK in tumor cells and tumor microenvironment: from function and mechanism to therapeutic application.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  18. Article
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Qin TangThe State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Wan LiThe State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Xiangjin ZhengThe State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Liwen RenThe State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Jinyi LiuThe State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Sha LiThe State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China.
Jinhua WangThe State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China. wjh@imm.ac.cn.
Guanhua DuThe State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, China. dugh@imm.ac.cn.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the fastest growth rate of morbidity and mortality in nearly a decade, and remains difficult to treat. Furthermore, the molecular mechanisms underlying its development are still unclear. In this study, bioinformatics analysis showed that MELK was highly expressed in lung cancer and negatively correlated to the survival of lung adenocarcinoma (LUAD). Immunohistochemistry analysis of LUAD patient tissues revealed there were a high level of MELK expression in LUAD. Knockdown of MELK expression inhibits the migration and invasion of LUAD cells, which may be mediated by Twist1, Slug, MMP7, and N-catenin. Overexpression of MELK promoted the growth of LUAD cells in medium, 3D Matrigel, and nude mice. Inhibition of MELK by OTSSP167 arrested cycle of LUAD cells at G2/M phase via PLK1-CDC25C-CDK1 pathway, and triggered apoptosis-mediated pyroptosis. Together, these data indicate that MELK is critical for metastasis, mitotic progression, and programmed death of LUAD and may be a promising therapeutic target for LUAD.

Indexed as

ApoptosisMitosisA549 CellsAdenocarcinoma of LungAnimalsHumansLung NeoplasmsMiceMice, NudeNeoplasm MetastasisNeoplasm ProteinsProtein Serine-Threonine KinasesMELK protein, humanNeoplasm ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID33262323
PMCPMC7708490
OpenAlexW3109862224

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.