Evidence map›Paper›PMID 20075984›Full record

ArticleCancer gene therapy2010

CUG2, a novel oncogene confers reoviral replication through Ras and p38 signaling pathway.

E-H Park, E H Park, I-R Cho, R Srisuttee, H-J Min, M-J Oh, Y-J Jeong, B H Jhun, R N Johnston, S Lee and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. A phase I trial of single-agent reolysin in patients with relapsed multiple myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
  15. Review
  16. Article
  17. Reovirus: a targeted therapeutic--progress and potential.Molecular cancer research : MCR · 2012
    Review
  18. Reovirus-associated reduction of microRNA-let-7d is related to the increased apoptotic death of cancer cells in clinical samples.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2012
    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

12 authors at 4 institutions in 2 countries.

E-H ParkDepartment of Cogno-Mechatronics Engineering, BK21 Nanofusion Technology Team, Pusan National University, Miryang, Republic of Korea.
E H Park
I-R Cho
R Srisuttee
H-J Min
M-J Oh
Y-J Jeong
B H Jhun
R N Johnston
S Lee
S S Koh
Y-H Chung
Pusan National University · KRKorea Research Institute of Bioscience and Biotechnology · KRChungnam National University · KRUniversity of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As we have recently found a novel oncogene, the cancer-upregulated gene 2 (CUG2), which was elevated in a variety of tumor tissues such as the ovary, liver, lung and pancreas, we examined whether reovirus could efficiently induce cytolysis in cancer cells expressing CUG2 and thus be used as a potential cancer therapeutic agent. In this study, we describe experiments in which we use reovirus to treat NIH3T3 cells stably expressing either CUG2 (NIH-CUG2) or vector only (NIH-Vec). NIH-CUG2 cells readily support reoviral proliferation and undergo apoptosis, whereas NIH-Vec cells are highly resistant to reoviral infection and virus-induced apoptosis. This notable result may be explained by the observation that CUG2 expression inhibits PKR activation, leading to reoviral proliferation in nonpermissive NIH3T3 cells. Furthermore, reovirus infection results in almost complete regression of tumorgenic NIH-CUG2 cells in transplanted nude mice. As we found that CUG2 enhances activation of MAPK (ERK, JNK and p38), Src kinase and Ras, we examined whether CUG2 confers reoviral replication independent of the Ras or p38 MAPK signaling pathway. From these experiments we found that either inhibition of p38 MAPK or Ras blocks reoviral proliferation even in the presence of CUG2 but inhibition of ERK, JNK and Src kinase does not, indicating that activation of p38 MAPK and Ras has critical roles in reoviral replication in CUG2-expressing tumor cells. Accordingly, we propose that reovirus can be useful in the treatment of transformed cells expressing CUG2, which is commonly detected in various tumor tissues.

Indexed as

AnimalsApoptosisBlotting, WesternCell LineChromosomal Proteins, Non-HistoneImmunohistochemistryIn Situ Nick-End LabelingMaleMiceMice, NudeNIH 3T3 CellsNuclear Proteinsp38 Mitogen-Activated Protein KinasesProliferating Cell Nuclear Antigenras ProteinsReoviridaeCENPW protein, humanChromosomal Proteins, Non-HistoneNuclear Proteinsp38 Mitogen-Activated Protein KinasesProliferating Cell Nuclear Antigenras Proteins

Identifiers

PMID20075984
OpenAlexW1966905733

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.