Evidence map›Paper›PMID 33745265›Full record

ArticleIranian biomedical journal2021

Interaction between LINC-ROR and Stemness State in Gastric Cancer Cells with Helicobacter pylori Infection.

Reihaneh Alsadat Mahmoudian, Maryam Lotfi Gharaie, Roya Abbaszadegan, Mohammad Mahdi Forghanifard, Mohammad Reza Abbaszadegan

Abstract read
In one paragraph

Article in Iranian biomedical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Advances inOncology letters · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Engagement of CEACAM1 byMicroorganisms · 2021
    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.

Reihaneh Alsadat MahmoudianImmunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Maryam Lotfi GharaieImmunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Roya AbbaszadeganImmunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Mohammad Mahdi ForghanifardDepartment of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran.
Mohammad Reza AbbaszadeganMedical Genetics Research Center, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLarge intergenic non-coding RNA regulator of reprogramming (LINC-ROR), as a cancer-related Long non-coding RNA, has vital roles in stem cell survival, pluripotency, differentiation, and self-renewal in human embryonic stem cell. However, cancer-related molecular mech¬anisms, its functional roles, and clinical value of LINC-ROR in gastric cancer (GC) remain unclear. In this study, we aimed to investigate probable interplay between LINC-ROR with SALL4 stemness regulator and their role with the development of the disease.

methodsThe mRNA expression profile of LINC-ROR and SALL4 was assessed in tumoral and adjacent non-cancerous tissues of GC patients, using quantitative real-time PCR.

resultsSignificant LINC-ROR underexpression and SALL4 overexpression were observed in 55.81% and 75.58% (p < 0.0001) of samples, respectively. The expression of LINC-ROR and SALL4 were significantly correlated with each other (p = 0.044). There was an association between the underexpression of LINC-ROR and sex, stage of tumor progression, tumor type, and location of tumor (p < 0.05), and Helicobacter pylori infection with SALL4 expression (p = 0.036). There were also significant correlations between concomitant mRNA expression of SALL4 and LINC-ROR in tumors located at distal noncardiac, positive for H. pylori infection, tumors with invasion into the muscle layer of the stomach, and grade II tumor (p < 0.05).

conclusionThe clinical results of the SALL4-LINC-ROR association propose a probable functional interaction between these markers in tumor maintenance and aggressiveness. Our study can help to understand one of the mechanisms involved in the progression of gastric cancer through the function of these regulators.

Identifiers

PMID33745265
PMCPMC8183384

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