Evidence map›Paper›PMID 32021259›Full record

ArticleOncoTargets and therapy2020

miR-1269b Drives Cisplatin Resistance of Human Non-Small Cell Lung Cancer via Modulating the PTEN/PI3K/AKT Signaling Pathway.

Wu Yang, Wei Xiao, Zhengrong Cai, Shidai Jin, Tian Li

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. miR-1269a and miR-1269b: Emerging Carcinogenic Genes of the miR-1269 Family.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Halofuginone Sensitizes Lung Cancer Organoids to CisplatinFrontiers in cell and developmental biology · 2021
    Article
  19. Article
  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 at 2 institutions in 1 country.

Wu YangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province 210029, People's Republic of China.
Wei XiaoDepartment of Radiotherapy, Nanjing Chest Hospital, Nanjing, Jiangsu Province 210029, People's Republic of China.
Zhengrong CaiDepartment of Respiratory Medicine, Nanjing Chest Hospital, Nanjing, Jiangsu Province 210029, People's Republic of China.
Shidai JinDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province 210029, People's Republic of China.
Tian LiDepartment of Respiratory Medicine, Nanjing Chest Hospital, Nanjing, Jiangsu Province 210029, People's Republic of China.
Nanjing Chest Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMiRNAs have been reported to induce certain drug resistance in multiple solid tumors via various mechanisms. Our study aimed to investigate whether miRNA-1269b was involved in the chemoresistance and the progression of non-small cell lung cancer (NSCLC).

methodsMTT and colony formation assay were conducted to determine cell proliferation and cell apoptosis was analyzed by flow cytometry with annexin V/PI. Luciferase reporter assay was performed to validate miRNA-targeting sequences. The function of miR-1269b in cisplatin-resistant was evaluated in vivo in a mouse tumor model.

resultsWe found that miR-1269b expression was up-regulated in cisplatin-resistant NSCLC specimens and NSCLC cell lines, which resulted in the promotion of chemoresistance and tumorigenicity. miR-1269b overexpression enhanced drug resistance and promoted cell proliferation in vitro and tumor growth in vivo, with reduced apoptosis rate of A549 cells inin vitro cell culture. Mechanistically, we identified PTEN as the direct target of miR-1269b, and the PTEN level was negatively correlated with miR-1269b in NSCLC specimens. Further study demonstrated that miR-1269b targeted PTEN to modulate PI3K/AKT signaling pathway.

conclusionIn conclusion, these findings suggest that the miR-1269b/PTEN/PI3K/AKT-mediated network might promote cisplatin resistance in NSCLC, and that miR-1269b can be a potential therapeutic target for chemoresistance in NSCLC patients.

Indexed as

cisplatin resistantmiR-1269bNSCLCPI3K/AKT signalingPTEN

Identifiers

PMID32021259
PMCPMC6954839
OpenAlexW2998421705

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.