Evidence map›Paper›PMID 35163030›Full record

ReviewInternational journal of molecular sciences2022

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma.

Lesley Jia Wei Pua, Chun-Wai Mai, Felicia Fei-Lei Chung, Alan Soo-Beng Khoo, Chee-Onn Leong, Wei-Meng Lim, Ling-Wei Hii

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 149 citations in OpenAlex.

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  14. New Phenylpropanoid fromCurrent pharmaceutical design · 2026
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26 more citing papers are in PubMed but not listed here.

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 1 country.

Lesley Jia Wei PuaSchool of Postgraduate Studies, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Chun-Wai MaiCenter for Cancer and Stem Cell Research, Development and Innovation (IRDI), Institute for Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.ORCID 0000-0001-6532-184X
Felicia Fei-Lei ChungDepartment of Medical Sciences, School of Medical and Life Sciences, Sunway University, Bandar Sunway 47500, Malaysia.ORCID 0000-0003-1043-4948
Alan Soo-Beng KhooCenter for Cancer and Stem Cell Research, Development and Innovation (IRDI), Institute for Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.ORCID 0000-0002-8268-5271
Chee-Onn LeongSchool of Postgraduate Studies, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.ORCID 0000-0002-6353-9703
Wei-Meng LimCenter for Cancer and Stem Cell Research, Development and Innovation (IRDI), Institute for Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Ling-Wei HiiCenter for Cancer and Stem Cell Research, Development and Innovation (IRDI), Institute for Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.ORCID 0000-0003-0537-3693
IMU University · MYSunway University · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) family members integrate signals that affect proliferation, differentiation, survival, and migration in a cell context- and cell type-specific way. JNK and p38 MAPK activities are found upregulated in nasopharyngeal carcinoma (NPC). Studies have shown that activation of JNK and p38 MAPK signaling can promote NPC oncogenesis by mechanisms within the cancer cells and interactions with the tumor microenvironment. They regulate multiple transcription activities and contribute to tumor-promoting processes, ranging from cell proliferation to apoptosis, inflammation, metastasis, and angiogenesis. Current literature suggests that JNK and p38 MAPK activation may exert pro-tumorigenic functions in NPC, though the underlying mechanisms are not well documented and have yet to be fully explored. Here, we aim to provide a narrative review of JNK and p38 MAPK pathways in human cancers with a primary focus on NPC. We also discuss the potential therapeutic agents that could be used to target JNK and p38 MAPK signaling in NPC, along with perspectives for future works. We aim to inspire future studies further delineating JNK and p38 MAPK signaling in NPC oncogenesis which might offer important insights for better strategies in diagnosis, prognosis, and treatment decision-making in NPC patients.

Indexed as

AnimalsAntineoplastic AgentsGene Expression Regulation, EnzymologicHumansJNK Mitogen-Activated Protein KinasesNasopharyngeal CarcinomaNasopharyngeal Neoplasmsp38 Mitogen-Activated Protein KinasesAntineoplastic AgentsJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein Kinasescancer cell survivalc-Jun N-terminal kinaseEpstein–Barr virusnasopharyngeal carcinomap38 mitogen-activated protein kinase

Identifiers

PMID35163030
PMCPMC8834850
OpenAlexW4205781555

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.