Evidence map›Paper›PMID 28766096›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2018

Inhibiting ERK/Mnk/eIF4E broadly sensitizes ovarian cancer response to chemotherapy.

S Liu, J Zha, M Lei

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

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  11. Targeting mTOR and eIF4E: a feasible scenario in ovarian cancer therapy.Cancer drug resistance (Alhambra, Calif.) · 2021
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  18. Deeping in the Role of the MAP-Kinases Interacting Kinases (MNKs) in Cancer.International journal of molecular sciences · 2020
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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

3 authors at 1 institution in 1 country.

S LiuDepartment of Ultrasound, The People's Hospital of Three Gorges University, The First People's Hospital of Yichang, Yichang, 443000, China. latte201217@163.com.ORCID http://orcid.org/0000-0002-8636-7334
J ZhaDepartment of Obstetrics and Gynecology, The People's Hospital of Three Gorges University, The First People's Hospital of Yichang, Yichang, 443000, China.
M LeiDepartment of Obstetrics and Gynecology, The People's Hospital of Three Gorges University, The First People's Hospital of Yichang, Yichang, 443000, China.
Yichang Central People's Hospital · CN

Funding

China Three Gorges University KJ2013B016
6 · The paper itself

Abstract

purposeTo investigate whether ERK/MNK/eIF4E contributes chemoresistance in ovarian cancer.

methodsThe phosphorylated levels of Erk, Mnk, and eIF4E were systematically analyzed in ovarian cancer patients before and after chemotherapy, and ovarian cancer cells exposed to short- and long-term chemo-agent treatment. The roles of Erk/Mnk/eIF4E were investigated using pharmacological and genetic approaches.

resultsIncreased phosphorylation levels of ERK, Mnk1, and eIF4E were observed in ovarian cancer cell exposed to chemotherapeutic agents, and paclitaxel-resistant SK-OV-3-r cells, and is a common response of ovarian cancer patients undergoing chemotherapy. MEK inhibitor U0126 inhibits basal and chemodrug-induced phosphorylation of ERK as well as Mnk1 and eIF4E, suggesting that Mnk1/eIF4E are the downstream signaling of ERK pathway and chemotherapy agents activate ERK/MNK/eIF4E in a MEK-dependent manner. eIF4E overexpression promotes ovarian cancer cell growth without affecting migration. In addition, ovarian cancer cells with eIF4E overexpression are more resistant to chemotherapeutic agents in aspect of growth inhibition and apoptosis induction compared to control cells. In contrast, eIF4E depletion augments chemotherapeutic agents' effect in ovarian cancer cells. These demonstrate that eIF4E play roles in growth and chemoresistance in ovarian cancer. MEK inhibitor U0126 also significantly enhances chemotherapeutic agents' inhibitory effects.

conclusionsOur work shows that ERK/Mnk/eIF4E activation is critically involved in ovarian cancer chemoresistance and inhibiting ERK/Mnk/eIF4E broadly sensitizes ovarian cancer response to chemotherapy.

Indexed as

Antineoplastic AgentsCopper-Transporting ATPasesDrug Resistance, NeoplasmFemaleHumansIntracellular Signaling Peptides and ProteinsNucleocytoplasmic Transport ProteinsOvarian NeoplasmsPhosphorylationProtein Serine-Threonine KinasesSignal TransductionAntineoplastic AgentsATP7A protein, humanCopper-Transporting ATPasesEIF4ENIF1 protein, humanIntracellular Signaling Peptides and ProteinsMKNK1 protein, humanNucleocytoplasmic Transport ProteinsProtein Serine-Threonine KinasesChemotherapy resistanceERKMnk/eIF4EOvarian cancer

Identifiers

PMID28766096
OpenAlexW2740089004

What OpenQuestion holds

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Registered trials

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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.