Evidence map›Paper›PMID 25842034›Full record

ArticleJournal of cancer research and clinical oncology2015

Downregulation of discoidin domain receptor 2 decreases tumor growth of hepatocellular carcinoma.

Joong-Won Park, Yeon-Su Lee, Jin Sook Kim, Sook-Kyung Lee, Bo Hyun Kim, Jung Ahn Lee, Nam Oak Lee, Seong Hoon Kim, Eun Kyung Hong

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2015. 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
1.2field-weighted citation impact, top 23% 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, 22 citations in OpenAlex.

  1. Review
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  8. Complex roles of discoidin domain receptor tyrosine kinases in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Review
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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

9 authors at 1 institution in 1 country.

Joong-Won ParkLiver and Pancreatobiliary Cancer Research Branch, National Cancer Center, Goyang, South Korea. jwpark@ncc.re.kr.
Yeon-Su LeeFunctional Genomics Branch, National Cancer Center, Goyang, South Korea. yslee2@ncc.re.kr.
Jin Sook KimLiver and Pancreatobiliary Cancer Research Branch, National Cancer Center, Goyang, South Korea. 73058@ncc.re.kr.
Sook-Kyung LeeLiver and Pancreatobiliary Cancer Research Branch, National Cancer Center, Goyang, South Korea. 73246@ncc.re.kr.
Bo Hyun KimCenter for Liver Cancer, National Cancer Center, 323 Ilsan-ro, Ilsan dong-gu, Goyang, Gyeonggi, 411-769, South Korea. bohkim@ncc.re.kr.
Jung Ahn LeeLiver and Pancreatobiliary Cancer Research Branch, National Cancer Center, Goyang, South Korea. chingal@hanmail.net.
Nam Oak LeeLiver and Pancreatobiliary Cancer Research Branch, National Cancer Center, Goyang, South Korea. leeno1752@naver.com.
Seong Hoon KimLiver and Pancreatobiliary Cancer Research Branch, National Cancer Center, Goyang, South Korea. kshlj@ncc.re.kr.
Eun Kyung HongLiver and Pancreatobiliary Cancer Research Branch, National Cancer Center, Goyang, South Korea. hongek@ncc.re.kr.
National Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDiscoidin domain receptors (DDRs) have been identified as tyrosine kinase receptors for collagen, and the overexpression of DDR1 was correlated with hepatocellular carcinoma (HCC) progression in vitro. Little is known about DDR2 on HCC cells, and we investigated the expression and function of DDR2 in human HCC cells.

methodsExpression of DDR2 in human HCC cell lines and patient HCC tissues was observed. The suppression of DDR2 by siRNA against DDR2 was performed in vitro and in vivo study.

resultsAll of HCC cell lines expressed DDR2 mRNA, and all HCC tissues from the ten patients with HCC demonstrated DDR2 mRNA expression. Transfection of DDR2 siRNA significantly inhibits cell growth compared to cells with nontarget siRNA transfection in vitro (P < 0.001). In SNU182, Hep3B, and HeLa cell xenograft models, there was a significant difference in average tumor volumes after 12 days of the DDR2 siRNA injection (P < 0.05) in SNU182 xenograft mice. DDR2 siRNA injection decreased the mean tumor volume by 65.6 % compared to that of the control. The apoptosis analysis demonstrated that DDR2 siRNA treatment significantly increased apoptotic cells (P < 0.01). Cell migration (P < 0.05) and cell invasion (P < 0.01) were significantly decreased by DDR2 siRNA treatment.

conclusionsThe inhibition of DDR2 by RNA interference suppressed in vivo and in vitro growth of human HCC cells. Our results may support that the use of DDR2 as a novel target of HCC treatment through control of tumor apoptosis, migration, and invasion.

Indexed as

3T3 CellsAnimalsApoptosisCarcinoma, HepatocellularCell AdhesionCell Line, TumorCell MovementCell ProliferationDiscoidin Domain ReceptorsDisease ProgressionHeLa CellsHumansLiver NeoplasmsMCF-7 CellsMiceMice, Inbred BALB CDiscoidin Domain ReceptorsReceptor Protein-Tyrosine KinasesReceptors, MitogenRNA, Small InterferingDDR2Growth inhibitionHepatocellular carcinoma

Identifiers

PMID25842034
PMCPMC11823954
OpenAlexW2060575870

What OpenQuestion holds

Textmetadata
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.