Evidence map›Paper›PMID 27822409›Full record

ArticleAmerican journal of cancer research2016

Autophagy inhibition promotes epithelial-mesenchymal transition through ROS/HO-1 pathway in ovarian cancer cells.

Zhe Zhao, Jing Zhao, Jing Xue, Xinrui Zhao, Peishu Liu

Abstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
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

43 citing papers in PubMed.

  1. Review
  2. Review
  3. Autophagy in Ovarian Cancer, an Opportunity or an Additional Threat?International journal of molecular sciences · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Heme Oxygenase-1 and Its Role in Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Deficiency ofFrontiers in immunology · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  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

5 authors.

Zhe ZhaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University 107 Wenhua Xi Road, Jinan 250012, Shandong, People's Republic of China.
Jing ZhaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University 107 Wenhua Xi Road, Jinan 250012, Shandong, People's Republic of China.
Jing XueDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University 107 Wenhua Xi Road, Jinan 250012, Shandong, People's Republic of China.
Xinrui ZhaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University 107 Wenhua Xi Road, Jinan 250012, Shandong, People's Republic of China.
Peishu LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University 107 Wenhua Xi Road, Jinan 250012, Shandong, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy has been proved to be involved in metastasis of cancers. However, the detailed mechanisms are still unclear. In this work, we aim to provide the first study of the role that autophagy plays in migration and invasion in ovarian cancer cells. Transwell chamber was used to examine migration and invasion capacities. Western blotting and immunofluorescence were performed to investigate the expressions of mesenchymal markers (Vimentin, N-cadherin), epithelial marker (Keratin), transcript factor (Zeb1) and HO-1. Small interfering RNA (siRNA) was used to generate autophagy defect cells (A2780 Atg7 siRNA and Skov-3 Atg7 siRNA cells). Reactive oxygen species (ROS) were examined by flow cytometry. We found Skov-3 cells exhibited a fibroblastoid like phenotype and more invasive ability with lower level of autophagy than A2780. Transwell chamber showed that autophagy inhibition promoted migration and invasion capacities of autophagy defect cells. Western blotting showed that the expressions of mesenchymal markers and transcript factor were up-regulated, while, the expression of epithelial marker was down-regulated in autophagy defect cells. Conversely, autophagy induction could impair the migration and invasion through reversing epithelial-mesenchymal transition (EMT) in A2780 and Skov-3 cells. Besides, autophagy defect could increase the level of intracellular ROS and the expression of HO-1. NAC (ROS scavenging agent) could inhibit the migration and invasion through reversing EMT and decrease the expression of HO-1. What's more, Znpp (HO-1 inhibitor) impaired the migration and invasion through reversing EMT. In conclusion, our results suggest that autophagy inhibition may promote EMT through ROS/HO-1 pathway in ovarian cancer cells.

Indexed as

Autophagy defectEMTHO-1ovarian cancerZeb1

Identifiers

PMID27822409
PMCPMC5088283

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.