Evidence map›Paper›PMID 30122894›Full record

ArticleDrug design, development and therapy2018

Doxorubicin-conjugated dexamethasone induced MCF-7 apoptosis without entering the nucleus and able to overcome MDR-1-induced resistance.

Kamontip Chaikomon, Supreecha Chattong, Theerasak Chaiya, Danai Tiwawech, Yongsak Sritana-Anant, Amornpun Sereemaspun, Krissanapong Manotham

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-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

15 citing papers in PubMed, 37 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Kamontip ChaikomonMolecular and Cellular Biology Unit, Department of Medicine, Lerdsin General Hospital, Bangkok, Thailand, kmanotham@hotmail.com.
Supreecha ChattongMolecular and Cellular Biology Unit, Department of Medicine, Lerdsin General Hospital, Bangkok, Thailand, kmanotham@hotmail.com.
Theerasak ChaiyaMolecular and Cellular Biology Unit, Department of Medicine, Lerdsin General Hospital, Bangkok, Thailand, kmanotham@hotmail.com.
Danai TiwawechResearch Division, National Cancer Institute, Bangkok, Thailand.
Yongsak Sritana-AnantDepartment of Chemistry, Faculty of Science, Chulalongkorn University, Bangkok, Thailand.
Amornpun SereemaspunDepartment of Anatomy, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Krissanapong ManothamMolecular and Cellular Biology Unit, Department of Medicine, Lerdsin General Hospital, Bangkok, Thailand, kmanotham@hotmail.com.
Lerdsin Hospital · THChulalongkorn University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDoxorubicin (DOX) is the most widely used chemotherapeutic agent that has multimodal cytotoxicity. The main cytotoxic actions of DOX occur in the nucleus. The emergence of drug-resistant cancer cells that have the ability to actively efflux DOX out of the nucleus, and the cytoplasm has led to the search for a more effective derivative of this drug. MATERIALS AND

methodsWe created a new derivative of DOX that was derived via simple conjugation of the 3' amino group of DOX to the dexamethasone molecule.

resultsDespite having a lower cytotoxic activity in MCF-7 cells, the conjugated product, DexDOX, exerted its actions in a manner that was different to that of DOX. DexDOX rapidly induced MCF-7 cell apoptosis without entering the nucleus. Further analysis showed that Dex-DOX increased cytosolic oxidative stress and did not interfere with the cell cycle. In addition, the conjugated product retained its cytotoxicity in multidrug resistance-1-overexpressing MCF-7 cells that had an approximately 16-fold higher resistance to DOX.

conclusionWe have synthesized a new derivative of DOX, which has the ability to overcome multidrug resistance-1-induced resistance. This molecule may have potential as a future chemotherapeutic agent.

Indexed as

Antineoplastic AgentsApoptosisATP Binding Cassette Transporter, Subfamily BCell CycleCell NucleusDexamethasoneDoxorubicinDrug Resistance, NeoplasmHumansMCF-7 CellsOxidative StressABCB1 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BDexamethasoneDoxorubicinbioconjugationdexamethasonedoxorubicindrug-resistant tumormultidrug resistancereactive oxygen species

Identifiers

PMID30122894
PMCPMC6078182
OpenAlexW2886191835

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.