Evidence map›Paper›PMID 31016558›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2019

Hypo-phosphorylated CD147 promotes migration and invasion of hepatocellular carcinoma cells and predicts a poor prognosis.

Jin Jin, Shi-Jie Wang, Jian Cui, Ling Li, Jia-Yue Li, Fen-Ling Liu, Xiu-Xuan Sun, Jian-Li Jiang, Hong-Yong Cui, Zhi-Nan Chen

Open access · hybridAbstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

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  8. The Heterogeneity of Liver Cancer Metabolism.Advances in experimental medicine and biology · 2021
    Article
  9. Article
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  11. CD147 promotes collective invasion through cathepsin B in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2020
    Article
  12. Article
  13. Article
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

10 authors at 2 institutions in 1 country.

Jin JinDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China.
Shi-Jie WangDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China.
Jian CuiState Key Laboratory of Pharmaceutical Biotechnology, Department of Biotechnology and Pharmaceutical Sciences, School of Life Sciences, Nanjing University, Nanjing, 210023, People's Republic of China.
Ling LiDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China.
Jia-Yue LiDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China.
Fen-Ling LiuDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China.
Xiu-Xuan SunDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China.
Jian-Li JiangDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China. jiangjl@fmmu.edu.cn.
Hong-Yong CuiDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China. cui-hongyong@163.com.
Zhi-Nan ChenDepartment of Cell Biology, National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, 710032, People's Republic of China. znchen@fmmu.edu.cn.
Air Force Medical University · CNNanjing University · CN

Funding

National Postdoctoral Program for Innovative Talents BX20180376National Science and Technology Major Project 2017ZX10203205-004-002Young Scientists Fund 31601127
6 · The paper itself

Abstract

purposeCD147 is a tumor-associated antigen that plays a key regulatory role in tumor invasion and distant metastasis. However, the exact role of CD147 phosphorylation, which is deregulated during cancer progression, is unknown. Here, the effects of CD147 phosphorylation on the malignant behavior of hepatocellular carcinoma (HCC) cells and its possible underlying mechanisms are explored.

methodsAn in situ Duolink-proximity ligation assay (PLA) was used to detect CD147 phosphorylation. Tandem mass spectrometry was employed to identify the phosphorylation sites of CD147. The effects of CD147 phosphorylation on the malignant behavior of HCC cells were evaluated using scratch wound healing assays, transwell invasion assays and cell cycle assays. The genes regulated by CD147 phosphorylation were detected by RNA sequencing.

resultsWe identified phosphorylated serine-246 in the C terminus of CD147 in primary HCC tissues, whereas serine to alanine substitution mutation analysis suggested that CD147 is phosphorylated mainly at serine-252 in HCC-derived Huh-7 cells. Recovery expression of S246A/S252A mutants in CD147 knockout cells revealed significantly increased migration and invasion capacities compared to wildtype CD147 expressing cells. Cyclophilin A (CyPA) treatment decreased the phosphorylation level of CD147, whereas NIMA-related kinase 6 (NEK6) increased the CD147 phosphorylation level. Moreover, the CD147 phosphorylation level was found to be dramatically decreased in HCC tissues in patients with distant metastases, and a low phosphorylation level of CD147 was found to be associated with a high serum AFP level, recurrence and a poor overall survival.

conclusionsFrom our data we conclude that hypo-phosphorylated CD147 promotes the migration and invasion of HCC cells and correlates with an unfavorable prognosis in HCC patients, indicating that targeting the aberrantly hypo-phosphorylated form of CD147 may be instrumental for the development of novel therapeutic modalities directed against HCC metastasis.

Indexed as

Cell MovementAmino Acid SequenceBasiginCarcinoma, HepatocellularCell Line, TumorCyclophilin AExtracellular MatrixFemaleGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleNeoplasm InvasivenessNeoplasm MetastasisNIMA-Related KinasesPhosphorylationBasiginBSG protein, humanCyclophilin ANEK6 protein, humanNIMA-Related KinasesPhosphoserineProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSTAT3 Transcription FactorCD147Hepatocellular carcinomaInvasionMetastasisPhosphorylation

Identifiers

PMID31016558
PMCPMC12994331
OpenAlexW2941415879

What OpenQuestion holds

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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.