Evidence map›Paper›PMID 28800701›Full record

ArticleIranian biomedical journal2018

A New Indole Derivative Decreased SALL4 Gene Expression in Acute Promyelocytic Leukemia Cell Line (NB4)

Zahra Sheikhrezaei, Parisa Heydari, Alireza Farsinezhad, Ahmad Fatemi, Soudeh Khanamani Falahati-Pour, Shokoofeh Darakhshan, Mojgan Noroozi Karimabad, Ali Darekordi, Hossein Khorramdelazad, Gholamhossein Hassanshahi

Open access · greenAbstract read
In one paragraph

Article in Iranian biomedical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022
    Review
  3. Knockdown ofAnnals of translational medicine · 2020
    Article
  4. Article
  5. Vanadium complex: an appropriate candidate for killing hepatocellular carcinoma cancerous cells.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2018
    Article
  6. Article
  7. Nisin Induces Cytotoxicity and Apoptosis in Human Asterocytoma Cell Line (SW1088)Asian Pacific journal of cancer prevention : APJCP · 2018
    Article
  8. Article
  9. Review
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 3 institutions in 1 country.

Zahra SheikhrezaeiDepartment of Hematology and Medical Laboratory Sciences, Faculty of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran.
Parisa HeydariDepartment of Hematology and Medical Laboratory Sciences, Faculty of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran.
Alireza FarsinezhadDepartment of Hematology and Medical Laboratory Sciences, Faculty of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran.
Ahmad FatemiDepartment of Hematology and Medical Laboratory Sciences, Faculty of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran.
Soudeh Khanamani Falahati-PourPistachio Safety Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Shokoofeh DarakhshanDepartment of Pediatrics, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Mojgan Noroozi KarimabadMolecular Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Ali DarekordiDepartment of Chemistry, Faculty of Science, Vali-E-Asr University of Rafsanjan, Rafsanjan, Iran.
Hossein KhorramdelazadMolecular Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Gholamhossein HassanshahiMolecular Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Rafsanjan University of Medical Sciences · IRKerman University of Medical Sciences · IRVali Asr University of Rafsanjan · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Acute myeloblastic leukemia (AML) is a clonal disorder due to bone marrow failure and uncontrolled proliferation of myeloid lineage. Acute promyelocytic leukemia (APL) is a subtype of AML. Heterocyclic compounds, such as indole, are considered as attractive candidates for cancer therapy, due to their abundance in nature and known biological activity. Sal-like protein (SALL4) is a zinc finger transcription factor involving in the multi-potency of stem cells, in the NB4 cell line. This study was aimed to evaluate the effects of basal indole and its new derivative, 2-(1-((2, 4-Aril)imino)-2,2,2-trifluoroethyl) phenyl-1H Indole-3- carbaldehyde (TFPHC), on the expression of SALL4. Methods: Cells were cultured and treated with different concentrations (75, 150, and 300 µg/mL) of the new indole derivative and DMSO, as a vehicle control, for 24 and 48 hours. Cell proliferation was evaluated by using Trypan blue exclusion and MTT assays. The percentage of apoptotic cells was determined by flowcytometry analysis using the Annexin V/PI apoptosis detection kit; mRNA expression of SALL4 was studied using absolute quantitative RT-PCR. Data were analyzed by student's t-test. P<0.05 were considered statistically significant. Results: Our findings demonstrated the effects of new indole derivatives on SALL4 mRNA expression. Expression of SALL4 mRNA was significantly decreased at 75, 150, and 300 µg/mL concentrations. Conclusion: SALL4 plays a role in the survival of APL cells. SALL4 expression could be suppressed by the novel indole derivative. Additionally, SALL4 gene suppression can serve as a target in APL therapy.

Indexed as

Acute promyelocyticIndolesLeukemiaSALL4 protein

Identifiers

PMID28800701
PMCPMC5786664
OpenAlexW2757237156

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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.