Evidence map›Paper›PMID 30627877›Full record

ArticleInvestigational new drugs2019

Inhibition of AKT signalling by benzoxazine derivative LTUR6 through the modulation of downstream kinases.

Rejitha Suraj, Jasim Al-Rawi, Christopher Bradley

Abstract read
PubMed Publisher
In one paragraph

Article in Investigational new drugs, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Cycloaddition of 4-Acyl-1Molecules (Basel, Switzerland) · 2022
    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.

Rejitha SurajFaculty of Science Technology and Engineering, School of Pharmacy and Applied Science, Latrobe Institute of Molecular Sciences, La Trobe University, Bendigo, Australia. rejitha.suraj@ucalgary.ca.
Jasim Al-RawiCollege of Science, Health and Engineering, La Trobe University, Bendigo, Australia.
Christopher BradleyFaculty of Science Technology and Engineering, School of Pharmacy and Applied Science, Latrobe Institute of Molecular Sciences, La Trobe University, Bendigo, Australia.
La Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many compounds structurally similar to chromones have been developed to enhance the sensitizing effect of cancer cells to chemotherapeutic agents. Most of these compounds have been shown to promote this sensitization by targeting the repair pathways. One such compound is LTUR6, which enhances the sensitization of doxorubicin to colon cancer cells HT29, by inhibiting the phosphorylation of the double stranded break (DSB) repair enzyme AKT. The downstream regulatory targets of AKT that enhance doxorubicin mediated cytotoxicity in the presence of LTUR6 remains elusive. In this study, we performed comparative analyses of 43 kinase phosphorylation sites using the human phospho-kinase array proteome profiler. Results revealed altered expression levels of multiple proteins that regulated apoptotic signalling pathways. Increased activation of mTOR, RSK1/2/3, p38α and PRAS40 after combination treatment with LTUR6 and doxorubicin over doxorubicin alone was observed. This study provides a deeper insight into the key proteins involved and presents a novel molecular pathway.

Indexed as

Antineoplastic AgentsBenzoxazinesDoxorubicinDrug InteractionsHT29 CellsHumansPhosphorylationProtein Kinase InhibitorsProtein KinasesProteomeSignal TransductionAntineoplastic AgentsBenzoxazinesDoxorubicinProtein Kinase InhibitorsProtein KinasesProteomeAKTApoptosisChemosensitizationDoxorubicin

Identifiers

PMID30627877
OpenAlexW2909480139

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.