Evidence map›Paper›PMID 29383135›Full record

ArticleOncotarget2017

Upregulation of RSPO2-GPR48/LGR4 signaling in papillary thyroid carcinoma contributes to tumor progression.

Yea Eun Kang, Jin-Man Kim, Koon Soon Kim, Joon Young Chang, Mingyu Jung, Junguee Lee, Shinae Yi, Hyeon Woo Kim, Jung Tae Kim, Kyungmin Lee and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. The Role of LGR4 (GPR48) in Normal and Cancer Processes.International journal of molecular sciences · 2021
    Review
  8. Review
  9. 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

16 authors at 2 institutions in 2 countries.

Yea Eun Kang *Department of Endocrinology and Metabolism, College of Medicine, Chungnam National University, Daejeon 35015, South Korea.
Jin-Man Kim *Department of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Koon Soon Kim *Department of Endocrinology and Metabolism, College of Medicine, Chungnam National University, Daejeon 35015, South Korea.
Joon Young ChangDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Mingyu JungDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Junguee LeeDepartment of Pathology, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Daejeon 34943, Republic of Korea.
Shinae YiDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Hyeon Woo KimDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Jung Tae KimDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Kyungmin LeeDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Min Jeong ChoiDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Seul Ki KangDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Seong Eun LeeDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Hyon-Seung YiDepartment of Endocrinology and Metabolism, College of Medicine, Chungnam National University, Daejeon 35015, South Korea.
Bon Seok KooDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Minho ShongDepartment of Endocrinology and Metabolism, College of Medicine, Chungnam National University, Daejeon 35015, South Korea.
Chungnam National University · KRThe Catholic University of Korea Daejeon St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The signaling pathway involving the R-spondins and its cognate receptor, GPR48/LGR4, is crucial in development and carcinogenesis. However, the functional implications of the R-spondin-GPR48/LGR4 pathway in thyroid remain to be identified. The aim of this study was to investigate the role of R-spondin-GPR48/LGR4 signaling in papillary thyroid carcinomas. We retrospectively reviewed a total of 214 patients who underwent total thyroidectomy and cervical lymph node dissection for papillary thyroid carcinoma. The role of GPR48/LGR4 in proliferation and migration was examined in thyroid cancer cell lines. R-spondin 2, and GPR48/LGR4 were expressed at significantly higher levels in thyroid cancer than in normal controls. Elevated GPR48/LGR4 expression was significantly associated with tumor size (P=0.049), lymph node metastasis (P=0.004), recurrence (P=0.037), and the BRAFV600E mutation (P=0.003). Moreover, high GPR48/LGR4 expression was an independent risk factor for lymph node metastasis (P=0.027) and the BRAFV600E mutation (P=0.009).

Indexed as

BRAFV600E mutationGPR48/LGR4papillary thyroid carcinomaRSPO2β-catenin pathway

Identifiers

PMID29383135
PMCPMC5777747
OpenAlexW2770361746

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.