Evidence map›Paper›PMID 34414106›Full record

ArticleFrontiers in oncology2021

Downregulated ARID1A by miR-185 Is Associated With Poor Prognosis and Adverse Outcomes in Colon Adenocarcinoma.

Salem Baldi, Hassan Khamgan, Yuanyuan Qian, Han Wu, Zhenyu Zhang, Mengyan Zhang, Yina Gao, Mohammed Safi, Mohammed Al-Radhi, Yun-Fei Zuo

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Molecular interplay of ARID1A in gastrointestinal cancers.Medical oncology (Northwood, London, England) · 2025
    Review
  2. Article
  3. Article
  4. The Prognostic and Therapeutic Potential of Fragile X Mental Retardation 1 (International journal of molecular sciences · 2024
    Article
  5. Article
  6. Review
  7. Relevance ofDiagnostics (Basel, Switzerland) · 2022
    Article
  8. Journal of Cancer · 2022
    Article
  9. Review
  10. Article
  11. 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

10 authors at 2 institutions in 2 countries.

Salem BaldiDepartment of Clinical Biochemistry, College of Laboratory Diagnostic Medicine, Dalian Medical University, Dalian, China.
Hassan KhamganDepartment of Molecular Diagnostics and Therapeutics, University of Sadat City, Sadat, Egypt.
Yuanyuan QianDepartment of Clinical Biochemistry, College of Laboratory Diagnostic Medicine, Dalian Medical University, Dalian, China.
Han WuDepartment of Clinical Biochemistry, College of Laboratory Diagnostic Medicine, Dalian Medical University, Dalian, China.
Zhenyu ZhangDepartment of Clinical Biochemistry, College of Laboratory Diagnostic Medicine, Dalian Medical University, Dalian, China.
Mengyan ZhangDepartment of Clinical Biochemistry, College of Laboratory Diagnostic Medicine, Dalian Medical University, Dalian, China.
Yina GaoDepartment of Clinical Biochemistry, College of Laboratory Diagnostic Medicine, Dalian Medical University, Dalian, China.
Mohammed SafiDepartment of Oncology, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Mohammed Al-RadhiDepartment of Urology, Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Yun-Fei ZuoDepartment of Clinical Biochemistry, College of Laboratory Diagnostic Medicine, Dalian Medical University, Dalian, China.
Dalian Medical University · CNUniversity of Sadat City · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AT-rich interaction domain 1A (ARID1A) is a tumor suppressor gene that mutates in several cancer types, including breast cancer, ovarian cancer, and colorectal cancer (CRC). In colon adenocarcinoma (COAD), the low expression of ARID1A was reported but the molecular reason is unclear. We noticed that ARID1A low expression was associated with increased levels of miR-185 in the COAD. Therefore, this study aims to explore ncRNA-dependent mechanism that regulates ARID1A expression in COAD regarding miR-185. The expression of ARID1A was tested in COAD cell line under the effect of miR-185 mimics compared with inhibitor. The molecular features associated with loss of ARID1A and its association with tumor prognosis were analyzed using multi-platform data from The Cancer Genome Atlas (TCGA), and gene set enrichment analysis (GSEA) to identify potential signaling pathways associated with ARID1A alterations in colon cancer. Kaplan-Meier survival curve showed that a low level of ARID1A was closely related to low survival rate in patients with COAD. Results showed that inhibiting miR-185 expression in the COAD cell line significantly restored the expression of ARID1A. Further, the increased expression of ARID1A significantly improved the prolonged overall survival of COAD. We noticed that there is a possible relationship between ARID1A high expression and tumor microenvironment infiltrating immune cells. Furthermore, the increase of ARID1A in tumor cells enhanced the response of inflammatory chemokines. In conclusion, this study demonstrates that ARID1A is a direct target of miR-185 in COAD that regulates the immune modulations in the microenvironment of COAD.

Indexed as

AT-rich interaction domain 1A (ARID1A)gene expressionimmune cell infiltrationmiR-185-5Pposttranscriptional regulationThe Cancer Genome Atlas (TCGA)

Identifiers

PMID34414106
PMCPMC8367751
OpenAlexW3191212934

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.