Evidence map›Paper›PMID 27888617›Full record

ArticleOncotarget2016

Suppression of osteopontin inhibits chemically induced hepatic carcinogenesis by induction of apoptosis in mice.

Su-Hyung Lee, Jun-Won Park, Sang-Ho Woo, Du-Min Go, Hyo-Jung Kwon, Ja-June Jang, Dae-Yong Kim

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Osteopontin promotes gastric cancer progressionWorld journal of gastrointestinal oncology · 2023
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Linkage of CD8Scientific reports · 2019
    Article
  9. Article
  10. Lack of galectin-1 exacerbates chronic hepatitis, liver fibrosis, and carcinogenesis in murine hepatocellular carcinoma model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
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 3 institutions in 1 country.

Su-Hyung LeeDepartment of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, South Korea.
Jun-Won ParkBiomolecular Function Research Branch, National Cancer Center, Goyang, Gyeonggi 410-769, South Korea.
Sang-Ho WooDepartment of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, South Korea.
Du-Min GoDepartment of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, South Korea.
Hyo-Jung KwonDepartment of Veterinary Pathology, College of Veterinary Medicine, Chungnam National University, Daejeon 305-764, South Korea.
Ja-June JangDepartment of Pathology, College of Medicine, Seoul National University, Seoul 110-799, Korea.
Dae-Yong KimDepartment of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, South Korea.
Seoul National University · KRChungnam National University · KRNational Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous clinical reports have found elevated osteopontin (OPN) levels in tumor tissues to be indicative of greater malignancy in human hepatocellular carcinoma (HCC). However, the role of OPN on carcinogenesis and its underlying mechanism remain unclear. In the present study, we investigated the oncogenic role of OPN in diethylnitrosamine (DEN)-induced hepatic carcinogenesis in mice. The overall incidence of hepatic tumors at 36 weeks was significantly lower in OPN knockout (KO) mice than in wild-type (WT) mice. Apoptosis was significantly enhanced in OPN KO mice, and was accompanied by the downregulation of epidermal growth factor receptor (EGFR). In the in vitro study, OPN suppression also led to lower mRNA and protein levels of EGFR associated with the downregulation of c-Jun in Hep3B and Huh7 human HCC cells lines, which resulted in increased apoptotic cell death in both cell lines. Moreover, a positive correlation was clearly identified between the expression of OPN and EGFR in human HCC tissues. These data demonstrate that the OPN deficiency reduced the incidence of chemically induced HCC by suppressing EGFR-mediated anti-apoptotic signaling. An important implication of our findings is that OPN positively contributes to hepatic carcinogenesis.

Indexed as

ApoptosisAnimalsCell Line, TumorDiethylnitrosamineErbB ReceptorsHumansLiver NeoplasmsMaleMiceMice, Inbred C57BLMice, KnockoutOsteopontinSignal TransductionDiethylnitrosamineErbB ReceptorsOsteopontinapoptosisc-JunEGFRhepatocellular carcinomaosteopontin

Identifiers

PMID27888617
PMCPMC5349983
OpenAlexW2549071489

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.