Evidence map›Paper›PMID 29219949›Full record

ArticleActa pharmacologica Sinica2018

A miRNA-200c/cathepsin L feedback loop determines paclitaxel resistance in human lung cancer A549 cells in vitro through regulating epithelial-mesenchymal transition.

Yi-Fan Zhao, Mei-Ling Han, Ya-Jie Xiong, Long Wang, Yao Fei, Xiao Shen, Ying Zhu, Zhong-Qin Liang

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. MiRNA-mediated EMT and CSCs in cancer chemoresistance.Experimental hematology & oncology · 2021
    Review
  17. Article
  18. A Compressive Review about TaxolMolecules (Basel, Switzerland) · 2020
    Review
  19. Review
  20. Review
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

8 authors at 1 institution in 1 country.

Yi-Fan ZhaoDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.
Mei-Ling HanDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.
Ya-Jie XiongDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.
Long WangDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.
Yao FeiDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.
Xiao ShenDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.
Ying ZhuDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.
Zhong-Qin LiangDepartment of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cathepsin L (CTSL), a cysteine protease, is closely related to tumor occurrence, development, and metastasis, and possibly regulates cancer cell resistance to chemotherapy. miRNAs, especially the miR-200 family, have been implicated in drug-resistant tumors. In this study we explored the relationship of CTSL, miRNA-200c and drug resistance, and the potential regulatory mechanisms in human lung cancer A549 cells and A549/TAX cells in vitro. A549/TAX cells were paclitaxel-resistant A549 cells overexpressing CTSL and characterized by epithelial-mesenchymal transition (EMT). We showed that miRNA-200c and CTSL were reciprocally linked in a feedback loop in these cancer cells. Overexpression of miRNA-200c in A549/TAX cells decreased the expression of CTSL, and enhanced their sensitivity to paclitaxel and suppressed EMT, whereas knockdown of miRNA-200c in A549 cells significantly increased the expression of CTSL, and decreased their sensitivity to paclitaxel and induced EMT. Overexpression of CTSL in A549 cells significantly decreased the expression of miRNA-200c, and reduced their sensitivity to paclitaxel and induced EMT, but these effects were reversed by miRNA-200c, whereas knockdown of CTSL in A549/TAX cells attenuated paclitaxel resistance and remarkably inhibited EMT, but the inhibition of miRNA-200c could reverse these effects. Therefore, miRNA-200c may be involved in regulating paclitaxel resistance through CTSL-mediated EMT in A549 cells, and CTSL and miRNA-200c are reciprocally linked in a feedback loop.

Indexed as

Drug Resistance, NeoplasmA549 CellsAntineoplastic Agents, PhytogenicCathepsin LCell MovementCell ProliferationDose-Response Relationship, DrugEpithelial-Mesenchymal TransitionFeedback, PhysiologicalGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsNeoplasm InvasivenessPaclitaxelSignal TransductionAntineoplastic Agents, PhytogenicCathepsin LCTSL protein, humanMicroRNAsMIRN200 microRNA, humanPaclitaxel

Identifiers

PMID29219949
PMCPMC6256272
OpenAlexW2774579990

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.