Evidence map›Paper›PMID 28093638›Full record

ArticleJournal of cancer research and clinical oncology2017

Depletion of p42.3 gene inhibits proliferation and invasion in melanoma cells.

Hui Liu, Min Zhu, Zhongwu Li, Yan Wang, Rui Xing, Youyong Lu, Weicheng Xue

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

12 citing papers in PubMed, 11 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 1 country.

Hui LiuDepartment of Pathology, Peking University Cancer Hospital and Institute, Beijing, 100142, China.
Min ZhuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital and Institute, Beijing, 100142, China.
Zhongwu LiDepartment of Pathology, Peking University Cancer Hospital and Institute, Beijing, 100142, China.
Yan WangDepartment of Pathology, Peking University Cancer Hospital and Institute, Beijing, 100142, China.
Rui XingKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital and Institute, Beijing, 100142, China.
Youyong LuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital and Institute, Beijing, 100142, China. youyonglu@sina.com.
Weicheng XueDepartment of Pathology, Peking University Cancer Hospital and Institute, Beijing, 100142, China. xuewc2004@aliyun.com.
Peking University · CNPeking University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe p42.3 gene is identified recently, and the upregulated expression has been characterized in a variety of human cancers and embryonic tissues but not yet in malignant melanoma. In this study, we explored the role of p42.3 gene in the development of melanoma.

methodsThe expression of p42.3 was detected by immunohistochemistry staining of 261 cases of patient lesions, including nevi and melanoma, and its correlation with clinical pathological characteristics and prognosis was analyzed. Furthermore, a series of in vitro assays were used to investigate the biological function of p42.3 in melanoma cells.

resultsImmunohistochemistry staining showed an elevated expression level of p42.3 in melanoma compared to nevi (P = 0.001). Statistical analysis indicated that this high level was well correlated with patients' clinical stage (P = 0.045), but not with gender, age, clinical type, mitotic rate, and overall survival (P > 0.05). Moreover, in vitro assays showed knockdown p42.3 gene expression could inhibit the biological profiling, including proliferation, migration, and invasion of melanoma cells, and also affect PI3K/Akt pathway, MAPK pathway, and β-catenin.

conclusionsThis study suggests that p42.3, acting like an oncogene, is involved in the malignant transformation process of melanoma and may serve as a biomarker for diagnostic and treatment purposes.

Indexed as

Cell Cycle ProteinsCell ProliferationFemaleGene SilencingHumansMaleMelanomaMiddle AgedNeoplasm InvasivenessNuclear ProteinsCell Cycle ProteinsNuclear ProteinsSAPCD2 protein, humanClinical stageMelanomaMigration and invasionp42.3 geneProliferation

Identifiers

PMID28093638
PMCPMC11819132
OpenAlexW2576480513

What OpenQuestion holds

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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.