Evidence map›Paper›PMID 37432950›Full record

ArticlePloS one2023

Dermokine mutations contribute to epithelial-mesenchymal transition and advanced melanoma through ERK/MAPK pathways.

Wenqiong Ma, Zexiu Wu, Mazaher Maghsoudloo, Iqra Ijaz, Marzieh Dehghan Shasaltaneh, Yuqin Zhang, Qiao Weng, Junjiang Fu, Saber Imani, Qing Lian Wen

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  5. Review
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 2 countries.

Wenqiong MaDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Zexiu WuDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Mazaher MaghsoudlooFaculty of Advanced Science and Technology, Department of Genetics, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Iqra IjazSichuan Provincial Center for Gynecological and Breast Diseases, Southwest Medical University, Luzhou, Sichuan, China.
Marzieh Dehghan ShasaltanehFaculty of Science, Department of Biology, University of Zanjan, Zanjan, Iran.
Yuqin ZhangDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Qiao WengDepartment of Obstetrics & Gynecology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China.
Junjiang FuKey Laboratory of Epigenetics and Oncology, The Research Center for Preclinical Medicine, Southwest Medical University, Luzhou, Sichuan, China.
Saber ImaniDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.ORCID 0000-0003-1308-8403
Qing Lian WenDepartment of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Affiliated Hospital of Southwest Medical University · CNSouthwest Medical University · CNIslamic Azad University Medical Branch of Tehran · IRNanjing Drum Tower Hospital · CNUniversity of Zanjan · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To discover vulnerabilities associated with dermokine (DMKN) as a new trigger of the epithelial-mesenchymal transition (EMT) -driven melanoma, we undertook a genome-wide genetic screening using transgenic. Here, we showed that DMKN expression could be constitutively increased in human malignant melanoma (MM) and that this correlates with poor overall survival in melanoma patients, especially in BRAF-mutated MM samples. Furthermore, in vitro, knockdown of DMKN inhibited the cell proliferation, migration, invasion, and apoptosis of MM cancer cells by the activation of ERK/MAPK signaling pathways and regulator of STAT3 in downstream molecular. By interrogating the in vitro melanoma dataset and characterization of advanced melanoma samples, we found that DMKN downregulated the EMT-like transcriptional program by disrupting EMT cortical actin, increasing the expression of epithelial markers, and decreasing the expression of mesenchymal markers. In addition, whole exome sequencing was presented with p.E69D and p.V91A DMKN mutations as a novel somatic loss of function mutations in those patients. Moreover, our purposeful proof-of-principle modeled the interaction of ERK with p.E69D and p.V91A DMKN mutations in the ERK-MAPK kinas signaling that may be naturally associated with triggering the EMT during melanomagenesis. Altogether, these findings provide preclinical evidence for the role of DMKN in shaping the EMT-like melanoma phenotype and introduced DMKN as a new exceptional responder for personalized MM therapy.

Indexed as

MelanomaSkin NeoplasmsCutaneous Malignant MelanomaEpithelial-Mesenchymal TransitionHumansIntercellular Signaling Peptides and ProteinsMutationDMKN protein, humanIntercellular Signaling Peptides and Proteins

Identifiers

PMID37432950
PMCPMC10335698
OpenAlexW4383875201

What OpenQuestion holds

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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.