Evidence map›Paper›PMID 27572899›Full record

ArticleMolecular medicine reports2016

Cabazitaxel-induced autophagy via the PI3K/Akt/mTOR pathway contributes to A549 cell death.

Ruichao Huo, Lili Wang, Peijuan Liu, Yong Zhao, Caiqin Zhang, Bing Bai, Xueying Liu, Changhong Shi, Sanhua Wei, Hai Zhang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Targeting PI3K/Akt signal transduction for cancer therapy.Signal transduction and targeted therapy · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Ruichao HuoCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi 712100, P.R. China.
Lili WangCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi 712100, P.R. China.
Peijuan LiuLaboratory Animal Center, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Yong ZhaoLaboratory Animal Center, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Caiqin ZhangLaboratory Animal Center, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Bing BaiLaboratory Animal Center, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Xueying LiuDepartment of Medicinal Chemistry, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Changhong ShiLaboratory Animal Center, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Sanhua WeiDepartment of Laboratory and Research Center, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Hai ZhangLaboratory Animal Center, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
Air Force Medical University · CNNorthwest A&F University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cabazitaxel has been used to treat castration-resistant prostate cancer since its approval by the US Food and Drug Administration in 2010. However, whether cabazitaxel may inhibit the proliferation of other tissue‑derived cancer cells, and its underlying mechanism, remains unknown. In the present study, the A549 lung adenocarcinoma cancer cell line was exposed to cabazitaxel, in order to investigate its cytotoxic effect and determine the underlying mechanism. The results demonstrated that cabazitaxel was able to induce autophagy in A549 cells, as evidenced by the formation of autophagosomes, upregulated LC3‑II expression and increased LC3 puncta. Cabazitaxel‑induced autophagy had a cytotoxic effect on A549 cells, as evidenced by the induction of cell death and cell cycle arrest at G2/M phase, which was independent of the apoptotic pathway. Furthermore, transfection with Beclin1 small interfering RNA and treatment with the autophagy inhibitor 3‑methyladenine protected cells from cabazitaxel‑induced cell death, thus confirming that cabazitaxel‑induced autophagy contributed to A549 cell death. In addition, cabazitaxel targeted the phosphoinositide 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway to induce autophagy, as indicated by reduced phosphorylation of Akt and mTOR. In conclusion, the present study demonstrated that cabazitaxel exerts a cytotoxic effect on A549 cells by acting on the PI3K/Akt/mTOR pathway to promote autophagic cell death. This result supports the potential use of cabazitaxel as a chemotherapeutic agent for the treatment of lung cancer.

Indexed as

A549 CellsAdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsApoptosisAutophagyHumansLungLung NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTaxoidsTOR Serine-Threonine KinasesAntineoplastic AgentscabazitaxelMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTaxoidsTOR Serine-Threonine Kinases

Identifiers

PMID27572899
PMCPMC5042750
OpenAlexW2512526160

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.