Evidence map›Paper›PMID 37891359›Full record

ArticleMedical oncology (Northwood, London, England)2023

Mechanism of anticancer effect of ETP-45658, a PI3K/AKT/mTOR pathway inhibitor on HT-29 Cells.

Fatih Yulak, Ahmet Kemal Filiz, Zıad Joha, Mustafa Ergul

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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

4 authors at 1 institution in 1 country.

Fatih YulakDepartments of Physiology, School of Medicine, Cumhuriyet University, Sivas, Turkey.
Ahmet Kemal FilizDepartments of Physiology, School of Medicine, Cumhuriyet University, Sivas, Turkey.
Zıad JohaDepartment of Pharmacology, Faculty of Pharmacy, Sivas Cumhuriyet University, Sivas, Turkey.
Mustafa ErgulDepartment of Biochemistry, Faculty of Pharmacy, Sivas Cumhuriyet University, Sivas, Turkey. m.ergul@yahoo.com.tr.ORCID https://orcid.org/0000-0003-4303-2996
Sivas Cumhuriyet Üniversitesi · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The PI3K pathway plays a crucial role in tumor cell proliferation across various cancers, including colon cancer, making it a promising treatment target. This study aims to investigate the antiproliferative activity of ETP-45658, a PI3K/AKT/mTOR pathway inhibitor, on colon cancer and elucidate the underlying mechanisms. HT-29 colon cancer cells were treated with varying doses of ETP 45658 and its cytotoxic effect assessed using the XTT cell viability assay.ELISA was also used to measure TAS, TOS, Bax, BCL-2, cleaved caspase 3, cleaved PARP, and 8-oxo-dG levels. Flow cytometry was performed to investigate apoptosis, cell cycle, caspase 3/7 activity, and mitochondrial membrane potential. Additionally, following the administration of DAPI (4,6-diamidino-2-phenylindole) dye, the cells were visualized using an immunofluorescence microscope. It was observed that ETP-45658 exerted a dose-dependent and statistically significant antiproliferative effect on HT-29 colon cancer cells. Further investigations using the IC

Indexed as

Colonic NeoplasmsProto-Oncogene Proteins c-aktApoptosisCaspase 3Cell Line, TumorCell ProliferationHT29 CellsHumansPhosphatidylinositol 3-KinasesPyrazolesPyrimidinesSignal TransductionTOR Serine-Threonine KinasesCaspase 3ETP 45658Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazolesPyrimidinesTOR Serine-Threonine KinasesAnticancerApoptosisCell cycleETP-45658PI3K/AKT/mTOR inhibition

Identifiers

PMID37891359
OpenAlexW4387969465

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.