Evidence map›Paper›PMID 33753875›Full record

ArticleProstate cancer and prostatic diseases2021

CASC11 promotes aggressiveness of prostate cancer cells through miR-145/IGF1R axis.

Ozel Capik, Fatma Sanli, Ali Kurt, Onur Ceylan, Ilknur Suer, Murat Kaya, Michael Ittmann, Omer Faruk Karatas

Abstract read
PubMed Publisher
In one paragraph

Article in Prostate cancer and prostatic diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Overexpression ofEuropean journal of breast health · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. A review on the role of CASC11 in cancers.Frontiers in cell and developmental biology · 2023
    Review
  16. 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

8 authors at 5 institutions in 2 countries.

Ozel CapikMolecular Biology and Genetics Department, Erzurum Technical University, Erzurum, Turkey.
Fatma SanliMolecular Biology and Genetics Department, Erzurum Technical University, Erzurum, Turkey.
Ali KurtDepartment of Pathology, Erzurum Faculty of Medicine, Health Sciences University, Erzurum, Turkey.
Onur CeylanDepartment of Pathology, Faculty of Medicine, Ataturk University, Erzurum, Turkey.
Ilknur SuerDepartment of Internal Medicine, Division of Medical Genetics, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Murat KayaDepartment of Internal Medicine, Division of Medical Genetics, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Michael IttmannDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, TX, USA.ORCID http://orcid.org/0000-0003-4802-0978
Omer Faruk KaratasMolecular Biology and Genetics Department, Erzurum Technical University, Erzurum, Turkey. faruk.karatas@erzurum.edu.tr.ORCID http://orcid.org/0000-0002-0379-2088
Erzurum Technical University · TRIstanbul University · TRAtatürk University · TRMichael E. DeBakey VA Medical Center · USSağlık Bilimleri Üniversitesi · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProstate cancer (PCa) is the most common malignancy diagnosed among men after lung cancer in developed countries. Investigation of the underlying molecular mechanisms of PCa is urgently needed in order to develop better therapeutic strategies and to reveal more effective therapeutic targets. In this study, we aimed at exploring the potential functions of CASC11 in association with miR-145 and IGF1R during the malignant progression of PCa cells.

methodsWe initially investigated the oncogenic potential of noncoding members of CASC gene family and analyzed the effects of CASC11 overexpression on proliferation, migration, and colony formation ability of DU145, LNCaP, and PC3 PCa cells. We, then, exprlored the association of CASC11, miR-145, and IGF1R expression and their impacts on PI3K/AKT/mTOR signaling pathway in in vitro models.

resultsIn silico analysis revealed that of the CASC family only CASC11 showed consistent results considering its differential expression as well as its association with the overall survival of patients. We demonstrated that ectopic overexpression of CASC11 significantly increased the proliferation, colony formation, and migration capacity in all three cell lines. CASC11 overexpression caused suppression of miR-145 and overexpression of IGF1R, leading to activation of PI3K/AKT/mTOR signaling pathway.

conclusionIn summary, we found that CASC11 is upregulated in PCa cells and clinical tumor samples in comparison to corresponding controls and revealed that ectopic CASC11 overexpression promotes cellular phenotypes associated with PCa progression through CASC11/miR-145/IGF1R axis.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBiomarkers, TumorCell ProliferationHumansMaleMicroRNAsPrognosisProstatic NeoplasmsReceptor, IGF Type 1RNA, Long NoncodingTumor Cells, CulturedBiomarkers, TumorIGF1R protein, humanlong noncoding RNA CASC11, humanMicroRNAsMIRN145 microRNA, humanReceptor, IGF Type 1RNA, Long Noncoding

Identifiers

PMID33753875
OpenAlexW3135977790

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.