Evidence map›Paper›PMID 36497331›Full record

ArticleCancers2022

NPFFR2 Contributes to the Malignancy of Hepatocellular Carcinoma Development by Activating RhoA/YAP Signaling.

Yuna Shin, Wonhee Jung, Mi-Yeon Kim, Dongjo Shin, Geun Hee Kim, Chun Ho Kim, Sun-Hoo Park, Eung-Ho Cho, Dong Wook Choi, Chul Ju Han and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  4. Review
  5. 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

13 authors at 1 institution in 1 country.

Yuna ShinTeam of Radiation Convergence Research, Korea Institute of Radiological & Medical Sciences, Seoul 01812, Republic of Korea.ORCID 0000-0002-6019-0358
Wonhee JungTeam of Radiation Convergence Research, Korea Institute of Radiological & Medical Sciences, Seoul 01812, Republic of Korea.
Mi-Yeon KimTeam of Radiation Convergence Research, Korea Institute of Radiological & Medical Sciences, Seoul 01812, Republic of Korea.
Dongjo ShinRadiological and Medico-Oncological Sciences, University of Science and Technology, Daejeon 34113, Republic of Korea.
Geun Hee KimTeam of Radiation Convergence Research, Korea Institute of Radiological & Medical Sciences, Seoul 01812, Republic of Korea.
Chun Ho KimTeam of Radiation Convergence Research, Korea Institute of Radiological & Medical Sciences, Seoul 01812, Republic of Korea.
Sun-Hoo ParkDepartment of Pathology, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Republic of Korea.
Eung-Ho ChoDepartment of Surgery, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Republic of Korea.
Dong Wook ChoiDepartment of Surgery, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Republic of Korea.
Chul Ju HanDepartment of Internal Medicine, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Republic of Korea.
Kee Ho LeeTeam of Radiation Convergence Research, Korea Institute of Radiological & Medical Sciences, Seoul 01812, Republic of Korea.
Sang-Bum KimDepartment of Surgery, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Republic of Korea.
Hyun Jin ShinTeam of Radiation Convergence Research, Korea Institute of Radiological & Medical Sciences, Seoul 01812, Republic of Korea.
Korea Institute of Radiological and Medical Sciences · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) are a diverse family of cell surface receptors implicated in various physiological functions, making them common targets for approved drugs. Many GPCRs are abnormally activated in cancers and have emerged as therapeutic targets for cancer. Neuropeptide FF receptor 2 (NPFFR2) is a GPCR that helps regulate pain and modulates the opioid system; however, its function remains unknown in cancers. Here, we found that NPFFR2 is significantly up-regulated in liver cancer and its expression is related to poor prognosis. Silencing of NPFFR2 reduced the malignancy of liver cancer cells by decreasing cell survival, invasion, and migration, while its overexpression increased invasion, migration, and anchorage-independent cell growth. Moreover, we found that the malignant function of NPFFR2 depends on RhoA and YAP signaling. Inhibition of Rho kinase activity completely restored the phenotypes induced by NPFFR2, and RhoA/F-Actin/YAP signaling was controlled by NPFFR2. These findings demonstrate that NPFFR2 may be a potential target for the treatment of hepatocellular carcinoma.

Indexed as

GPCRhepatocellular carcinomainvasionmigrationNPFFNPFFR2RhoAYAP

Identifiers

PMID36497331
PMCPMC9737590
OpenAlexW4310057070

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.