Evidence map›Paper›PMID 31378128›Full record

ArticleCell cycle (Georgetown, Tex.)2019

CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer.

Yong Bai, Guojun Zhang, Ruirui Cheng, Rui Yang, Heying Chu

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. METTL14-mediated mInternational ophthalmology · 2025
    Article
  7. Article
  8. Review
  9. Lncrna CASC15 Activated By TCF12 Promote Colorectal Cancer ProgressionCombinatorial chemistry & high throughput screening · 2024
    Article
  10. Article
  11. Expression and Significance of LINC02418 in Breast Cancer.Breast cancer (Dove Medical Press) · 2024
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. A diagnostic and predictive lncRNAMolecular therapy. Nucleic acids · 2022
    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

5 authors at 1 institution in 1 country.

Yong BaiDepartment of Respiratory, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , P. R. China.
Guojun ZhangDepartment of Respiratory, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , P. R. China.
Ruirui ChengDepartment of Respiratory, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , P. R. China.
Rui YangDepartment of Respiratory, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , P. R. China.
Heying ChuDepartment of Respiratory, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , P. R. China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) are key mediators of cancer. The dysregulation of a lncRNA, CASC15, has been linked to several cancers, except lung cancer. Here, the aim of the study was to explore the role and mechanism of CASC15 in lung cancer regulation, with the focus on its interaction with a potential target, microRNA-766-5p (miR-766-5p) and an oncogene, kallikrein-related peptidase 12 (KLK12). Quantitative real-time PCR (qRT-PCR) was used to assess levels of CASC15, miR-766-5p and KLK12 in lung cancer tissues or cells. Western blot analysis was used to detect KLK12 protein expression. Ectopic expression of CASC15 was induced by a lentiviral system. CCK-8 and transwell assays were used to evaluate lung cancer cell proliferation and invasion, respectively. The interaction among CASC15, miR-766-5p and KLK12 was investigated by bioinformatical analysis and luciferase assay. In lung cancer tissue and cells, CASC15 was upregulated, while miR-766-5p was downregulated. Overexpression of CASC15 promoted lung cancer cell proliferation and invasion. A negative correlation was found between CASC15 and miR-766-5p levels. Overexpression of miR-766-6p reversed the cancer-promoting role of CASC15 in lung cancer cells, which was mediated by KLK12. The tumor-promoting role of CASC15 and tumor-suppressing role of miR-766-5p were also validated in vivo in tumor bearing mice, and KLK12 was also shown as an important mediator. CASC15 promotes lung cancer through the miR-766-5p/KLK12 axis, indicating that CASC15 is a potential therapeutic in lung cancer.

Indexed as

A549 CellsAlveolar Epithelial CellsAnimalsCell ProliferationGene Expression Regulation, NeoplasticHeterograftsHumansKallikreinsLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMicroRNAsNeoplasm InvasivenessRNA, Long NoncodingTransfectionKallikreinsKLK12 protein, humanMicroRNAsMIRN766 microRNA, humanRNA, Long NoncodingCASC15Lung cancermiR-766-5p/KLK12

Identifiers

PMID31378128
PMCPMC6738530
OpenAlexW2965599222

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.