Evidence map›Paper›PMID 31485224›Full record

ArticleJournal of oncology2019

YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A.

Eun Ji Kim, Mi Kyung Park, Gyeoung-Jin Kang, Hyun Jung Byun, Hyun Ji Kim, Lu Yu, Boram Kim, Hee-Sung Chae, Young-Won Chin, Jae Gal Shim and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Resolvin D1 Suppresses HAntioxidants (Basel, Switzerland) · 2021
    Article
  3. Article
  4. 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

12 authors at 2 institutions in 1 country.

Eun Ji KimPharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.
Mi Kyung ParkGraduate School of Cancer Science and Policy, National Cancer Center, Goyang, 10408, Republic of Korea.
Gyeoung-Jin KangPharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.
Hyun Jung ByunPharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.
Hyun Ji KimPharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.
Lu YuPharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.
Boram KimPharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.
Hee-Sung ChaePharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.
Young-Won ChinPharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.ORCID https://orcid.org/0000-0001-6964-1779
Jae Gal ShimGraduate School of Cancer Science and Policy, National Cancer Center, Goyang, 10408, Republic of Korea.
Ho LeeGraduate School of Cancer Science and Policy, National Cancer Center, Goyang, 10408, Republic of Korea.
Chang Hoon LeePharmaceutical Biochemistry, College of Pharmacy, Dongguk University, Seoul, Goyang, 04620, Republic of Korea.ORCID https://orcid.org/0000-0003-2210-0793
Dongguk University · KRNational Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the number 1 cause of cancer-related casualties in the world. Appropriate diagnostic markers and novel targets for lung cancer are needed. Chitooligosaccharide deacetylase homolog (YDJC) catalyzes the deacetylation of acetylated carbohydrates; however, the role of YDJC in lung cancer progression has yet to be studied. A549 lung cancer orthotopic mouse model was used for mice experiments. We found that YDJC overexpression contributes to lung cancer progression in an orthotopic mouse model. Long-term treatment (48 h) induces YDJC expression in sphingosylphosphorylcholine (SPC)-induced epithelial-mesenchymal transition (EMT). Gene silencing of YDJC (siYDJC) reduced N-cadherin expression and increased E-cadherin expression in SPC-induced EMT. Overexpression of YDJC reverses them but overexpression of the deacetylase deficient mutant YDJC

Identifiers

PMID31485224
PMCPMC6702825
OpenAlexW2964496943

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.