Evidence map›Paper›PMID 31602323›Full record

ArticleJournal of gastrointestinal oncology2019

Loss of ferrochelatase is protective against colon cancer cells: ferrochelatase a possible regulator of the long noncoding RNA H19.

Rémi Safi, Tala Mohsen-Kanson, Georges Nemer, Batoul Dekmak, Nelly Rubeiz, Marwan El-Sabban, Dany Nassar, Assaad Eid, Ossama Abbas, Abdul-Ghani Kibbi and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Journal of gastrointestinal oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. LOC101060264 Silencing Suppresses Invasion and Metastasis of Human Colon Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  7. 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

11 authors at 2 institutions in 1 country.

Rémi SafiDepartment of Dermatology, American University of Beirut, Beirut, Lebanon.
Tala Mohsen-KansonDepartment of Biology, Faculty of Sciences, Lebanese University, Zahle, Lebanon.
Georges NemerDepartment of Biochemistry and Molecular Genetics, American University of Beirut, Beirut, Lebanon.
Batoul DekmakAmerican University of Beirut, Beirut, Lebanon, Cell biology and Physiology, American University of Beirut, Beirut, Lebanon.
Nelly RubeizDepartment of Dermatology, American University of Beirut, Beirut, Lebanon.
Marwan El-SabbanDepartment of Anatomy, Cell biology and Physiology, American University of Beirut, Beirut, Lebanon.
Dany NassarDepartment of Dermatology, American University of Beirut, Beirut, Lebanon.
Assaad EidDepartment of Anatomy, Cell biology and Physiology, American University of Beirut, Beirut, Lebanon.
Ossama AbbasDepartment of Dermatology, American University of Beirut, Beirut, Lebanon.
Abdul-Ghani KibbiDepartment of Dermatology, American University of Beirut, Beirut, Lebanon.
Mazen KurbanDepartment of Dermatology, American University of Beirut, Beirut, Lebanon.
American University of Beirut · LBLebanese University · LB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFerrochelatase (FECH) is the last enzyme of the heme biosynthesis pathway. Deficiency in FECH was associated with many diseases, including protoporphyria. Correlation studies showed that variations of FECH expression was detected in human carcinomas and more specifically in colon cancer. Nevertheless, the potential role of FECH in colon cancer carcinogenesis

methodsA small interfering RNA (siRNA) was used to knockdown FECH in human Caco-2 colon cancer cells. The effect of FECH down-regulation on the cellular proliferation, the migration and the expression of target genes was assessed in cancer cells and compared to human normal fibroblasts.

resultsFollowing FECH down-regulation, our results demonstrated that the proliferation of Caco-2 cells was not affected. Furthermore, the migration of cancer and normal cells was affected, only when an additional stress factor (H

conclusionsIn conclusion, we showed that loss of FECH is protective against colon cancer tumorigenesis

Indexed as

colon cancerFerrochelatase (FECH)fibroblastsH19hypoxia

Identifiers

PMID31602323
PMCPMC6776811
OpenAlexW2940541495

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.