Evidence map›Paper›PMID 35059869›Full record

ArticleMedical oncology (Northwood, London, England)2022

The inhibition of Panc1 cancer cells invasion by hAMSCs secretome through suppression of tyrosine phosphorylation of SGK223 (at Y411 site), c-Src (at Y416, Y530 sites), AKT activity, and JAK1/Stat3 signaling.

Fatemeh Safari, Nasim Shafiee Nejad, Azadeh Aghaei Nejad

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Principles of Indirect Co-culture Method Using Transwell.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  5. Principles of Hanging Drop Method (Spheroid Formation) in Cell Culture.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  6. Article
  7. Article
  8. Therapeutic effects of hAMSCs secretome on proliferation of MDA-MB-231 breast cancer cells by the cell cycle arrest in G1/S phase.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    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

3 authors at 1 institution in 1 country.

Fatemeh SafariDepartment of Biology, Faculty of Science, University of Guilan, Rasht, Iran. fsafari@guilan.ac.ir.ORCID http://orcid.org/0000-0003-0300-7665
Nasim Shafiee NejadDepartment of Biology, Faculty of Science, University of Guilan, Rasht, Iran.
Azadeh Aghaei NejadDepartment of Biology, University Campus 2, University of Guilan, Rasht, Iran.
University of Guilan · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SGK223 is a scaffolding protein involving in the oncogenic tyrosine kinase signaling. SGK223 was phosphorylated at Y411 by c-Src and in response to the Epidermal growth factor receptor (EGFR). Tyrosine phosphorylated SGK223 at Y411 enables to interact with CSK resulting up regulation of c-Src activity and promotion of the cell migration. Human amniotic mesenchymal stromal cells (hAMSCs) are a population of multipotent cells that it was considered to be as a potential platform in cancer therapy. Herein, we employed a co-culture system to clarify the effects of hAMSCs secretome through tyrosine phosphorylation of c-Src, SGK223, AKT activity, and JAK1/Stat3 signaling in Panc1 pancreatic cancer cells. By using the 0.4 μm pore sized transwell membranes, both cell lines were firstly co-cultured for 72 h. Next, c-Src activity (tyrosine phosphorylation levels at Y530 and Y416), tyrosine phosphorylation level of SGK223 (at Y411), AKT activity, and JAK1/Stat3 signaling in Panc1 cells after treatment with hAMSCs were evaluated. Our results showed that hAMSCs have the inhibitory effects on Panc1 pancreatic cancer cells invasion and it suggests that the suppression of c-Src activity, SGK223 expression, AKT activity, and JAK1/Stat3 signaling may be as critical targets in pancreatic cancer therapy.

Indexed as

Cell Line, TumorCSK Tyrosine-Protein KinaseHumansIntracellular Signaling Peptides and ProteinsJanus Kinase 1Mesenchymal Stem CellsPancreatic NeoplasmsPhosphorylationReal-Time Polymerase Chain ReactionSecretomeSignal TransductionCSK Tyrosine-Protein KinaseIntracellular Signaling Peptides and ProteinsJAK1 protein, humanJanus Kinase 1PRAG1 protein, humanAKTJAK1/Stat3 signalingPancreatic cancer cellsSGK223Stem cells

Identifiers

PMID35059869
OpenAlexW4205725774

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.