Evidence map›Paper›PMID 35657703›Full record

ArticleCancer science2022

CD73 facilitates invadopodia formation and boosts malignancy of head and neck squamous cell carcinoma via the MAPK signaling pathway.

Feifei Xue, Tianxiao Wang, Hao Shi, Hongjie Feng, Guanying Feng, Ruixia Wang, Yao Yao, Hua Yuan

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. 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
2.6field-weighted citation impact, top 11% 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, 18 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

8 authors at 2 institutions in 1 country.

Feifei XueJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Tianxiao WangJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Hao ShiJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Hongjie FengJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Guanying FengJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Ruixia WangJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Yao YaoDepartment of Head and Neck Surgery, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China.
Hua YuanJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.ORCID https://orcid.org/0000-0002-5855-2196
Nanjing Medical University · CNJiangsu Cancer Hospital · CN

Funding

Key Project of Health Commission of Jiangsu Province ZDB202001LIUGEYI Project LGY2019088National Natural Science Foundation of China 81672678Open Project from Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University JSKLOD-KF-2105Priority Academic Program Development of Jiangsu Higher Education Institutions PAPD, 2018-87Project of Health Commission of Jiangsu Province H2019034
6 · The paper itself

Abstract

Elevated adenosine generated by CD73 (ecto-5'-nucleotidase; NT5E) could boost immunosuppressive responses and promote immune evasion in the tumor microenvironment. However, despite the immune response, CD73 could also promote tumor progression in a variety of cancers, and the nonimmunologic role and corresponding molecular mechanism of CD73 involved in head and neck squamous cell carcinoma (HNSCC) progression are not well characterized. Here, we demonstrated that CD73/NT5E is overexpressed in HNSCC tissues and predicts poor prognosis. Suppression of CD73 inhibited the proliferation, migration, and invasion of HNSCC cell lines (CAL27 and HN4) in vitro and in vivo. Gene set variation analysis (GSVA) and gene set enrichment analysis (GSEA) predicted that CD73 may be involved in invadopodia formation and MAPK signaling activation. As expected, knockdown of CD73 inhibited the MAPK signaling pathway, and the suppressive effect of CD73 knockdown on proliferation, migration, invasion, and invadopodia formation was reversed by a MAPK signaling activator. Our results suggest that CD73 could promote the proliferation, migration, invasion, and invadopodia formation of HNSCC via the MAPK signaling pathway and provide new mechanistic insights into the nonimmunological role of CD73 in HNSCC.

Indexed as

5'-NucleotidaseHead and Neck NeoplasmsPodosomesSquamous Cell Carcinoma of Head and NeckCell Line, TumorCell MovementCell ProliferationGPI-Linked ProteinsHumansSignal TransductionTumor Microenvironment5'-NucleotidaseGPI-Linked ProteinsNT5E protein, humanCD73EMTHNSCCinvadopodiaMAPK signaling pathway

Identifiers

PMID35657703
PMCPMC9357645
OpenAlexW4281741687

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.