Evidence map›Paper›PMID 27429846›Full record

ArticleAmerican journal of cancer research2016

Oncogenic miR-137 contributes to cisplatin resistance via repressing CASP3 in lung adenocarcinoma.

Te-Jen Su, Wen-Hui Ku, Hsuan-Yu Chen, Yi-Chiung Hsu, Qi-Sheng Hong, Gee-Chen Chang, Sung-Liang Yu, Jeremy Jw Chen

Open access · greenAbstract 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. miR-137: a potential therapeutic target for lung cancer.Frontiers in cell and developmental biology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. miR-137 functions as a tumor suppressor gene in pituitary adenoma by targeting AKT2.International journal of clinical and experimental pathology · 2019
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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 2 institutions in 1 country.

Te-Jen SuInstitute of Biomedical Sciences, National Chung-Hsing UniversityTaichung, Taiwan; Center of Genomic Medicine, National Taiwan UniversityTaipei, Taiwan.
Wen-Hui KuDepartment of Clinical Pathology, Taipei Institute of Pathology Taiwan.
Hsuan-Yu ChenInstitute of Statistical Science, Academia Sinica Taipei, Taiwan.
Yi-Chiung HsuInstitute of Statistical Science, Academia Sinica Taipei, Taiwan.
Qi-Sheng HongDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University Taipei, Taiwan.
Gee-Chen ChangDivision of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital Taichung, Taiwan.
Sung-Liang YuCenter of Genomic Medicine, National Taiwan UniversityTaipei, Taiwan; Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan UniversityTaipei, Taiwan.
Jeremy Jw ChenInstitute of Biomedical Sciences, National Chung-Hsing UniversityTaichung, Taiwan; Agricultural Biotechnology Center, National Chung Hsing UniversityTaichung, Taiwan; Rong Hsing Research Center for Translational Medicine, National Chung Hsing UniversityTaichung, Taiwan.
Institute of Statistical Science, Academia Sinica · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although targeted therapy can prolong the survival of non-small cell lung cancer (NSCLC) patients with EGFR mutations, chemotherapy still is the choice for patients with wild-type EGFR or failure in targeted therapy. However, most of the patients will eventually develop chemoresistance. Our previous study showed that miR-137 is a risky microRNA and is associated with poor prognosis in NSCLC patients. Here we investigated the role of miR-137 in cisplatin resistance in lung adenocarcinoma patients. Our data indicated that miR-137 overexpression increases the survival of lung cancer cells exposed to cisplatin and decreases cisplatin-induced apoptosis. Through computational prediction and microarray, we identified caspase-3 (CASP3) as a potential target of miR-137. Luciferase reporter and site-directed mutagenesis assays demonstrated that miR-137 downregulates CASP3 through binding to its 3'-UTR. Moreover, the endogenous CASP3 can be modulated by overexpressing or silencing miR-137 in lung adenocarcinoma cell lines regardless of EGFR status. Suppression of CASP3 by miR-137 provides cancer cells with anti-apoptotic ability, leading to cisplatin resistance. Immunohistochemistry results revealed an inverse correlation between miR-137 and CASP3 expressions in lung adenocarcinoma patients. Together, our data provide a new chemoresistance mechanism in lung adenocarcinoma and a possible target to control chemoresistance in lung adenocarcinoma patients.

Indexed as

caspase 3chemoresistancecisplatinlung adenocarcinomamiR-137

Identifiers

PMID27429846
PMCPMC4937735
OpenAlexW2475705639

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.