Evidence map›Paper›PMID 28401017›Full record

ArticleAmerican journal of cancer research2017

miR-495 promotes the chemoresistance of SCLC through the epithelial-mesenchymal transition via Etk/BMX.

Ting Wei, Weiliang Zhu, Shun Fang, Xiangpin Zeng, Jie Huang, Jie Yang, Jian Zhang, Linlang Guo

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Targeting the BMX in cancer: molecular mechanisms and emerging therapeutic strategies.Journal of enzyme inhibition and medicinal chemistry · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Non-Coding RNAs as Key Regulators in Lung Cancer.International journal of molecular sciences · 2023
    Review
  7. MicroRNA-495: a therapeutic and diagnostic tumor marker.Journal of molecular histology · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. [miR-203 inhibits lung cancer cell metastasis by targeting fatty acid binding protein 4].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
  15. Article
  16. Article
  17. 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.

Ting WeiDepartment of Oncology, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Weiliang ZhuDepartment of Oncology, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Shun FangDepartment of Pathology, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Xiangpin ZengDepartment of Gynaecology, Baoan Maternal and Child Health Hospital Shenzhen, China.
Jie HuangDepartment of Pathology, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Jie YangDepartment of Pathology, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Jian ZhangDepartment of Oncology, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Linlang GuoDepartment of Pathology, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Zhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

miR-495 serves as an oncogenic miRNA or a tumor suppressor in different types of cancer. However, its role in the drug resistance of small cell lung cancer (SCLC) remains unidentified. In this study, we investigated whether miR-495 regulates the chemoresistance of SCLC through the epithelial-mesenchymal transition (EMT) via Epithelial and endothelial tyrosine kinase (Etk/BMX) using two drug-resistant cell lines. Loss- and gain-of-function experiments showed miR-495 regulated cell proliferation, tumor growth and drug resistance. miR-495 suppression or Etk/BMX elevation in SCLC specimens was correlated with poor pathologic stage and survival time. Etk/BMX was one of the directly targeted genes of miR-495. Ectopic expression of Etk/BMX obviously rescued the miR-495 elevation elevation-induced inhibition of drug resistance. Etk/BMX over-expression led to higher levels of EMT mesenchymal factors (Zeb-2, Twist, Vim) and lower levels of the epithelial molecule β-catenin, while suppression of Etk/BMX showed the opposite trend. Knockdown of Zeb-2 and Twist inhibited the chemoresistance of cells. Our study revealed that miR-495 promoted the chemoresistance of SCLC through the epithelial-mesenchymal transition via Etk/BMX. miR-495 re-expression or Etk/BMX depletion is a promising strategy for interfering with chemoresistance in SCLC.

Indexed as

ChemoresistanceEMTEtk/BMXmiR-495SCLC

Identifiers

PMID28401017
PMCPMC5384991
OpenAlexW2996975762

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.