Evidence map›Paper›PMID 29212217›Full record

ArticleOncotarget2017

TMED2 promotes epithelial ovarian cancer growth.

Gong Shi-Peng, Chen Chun-Lin, Wu Huan, Meng Fan-Liang, Chen Yong-Ning, Zhang Ya-Di, Zhang Guang-Ping, Cai Ye-Ping

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 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
0.7field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. TMED family genes and their roles in human diseases.International journal of medical sciences · 2023
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. TMED2 as a marker of prognosis in breast cancer [Letter].Cancer management and research · 2019
    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

8 authors at 4 institutions in 1 country.

Gong Shi-PengDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China.
Chen Chun-LinDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China.
Wu HuanDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital, Chongqing University of Medical Sciences, Chongqing 400010, P.R. China.
Meng Fan-LiangDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China.
Chen Yong-NingDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China.
Zhang Ya-DiDepartment of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China.
Zhang Guang-PingDepartment of Gynecology, People's Hospital of Huadu District, Guangzhou 510800, P.R. China.
Cai Ye-PingDepartment of Gynecology, Maternal and Child Health Hospital of Duanzhou District, Zhaoqing 526000, P.R. China.
Nanfang Hospital · CNChongqing Maternal and Child Health Hospital · CNChongqing Medical University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TMED2 is involved in morphogenesis of the mouse embryo and placenta. We found that expression of TMED2 was higher in epithelial ovarian cancer tissues than normal ovarian tissues. Silencing TMED2 decreased cell proliferation, migration, and invasion. Ectopic expression of TMED2 increased cell proliferation, migration and invasion. Silencing TMED2 inhibited ovarian cancer growth in mice. Silencing TMED2 inhibited IGF2/IGF1R/PI3K/Akt pathway. In agreement, ectopically expressed TMED2 activated IGF2/IGF1R/PI3K/Akt pathway. Mechanistic study revealed that TMED2 directly binds to AKT2, thereby facilitating its phosphorylation. We also found that TMED2 increased IGF1R expression by competing for miR-30a. Thus, TMED2 is oncogenic and a potential target for epithelial ovarian cancer therapy.

Indexed as

AKTepithelial ovarian cancerIGF1RmiR-30aTMED2

Identifiers

PMID29212217
PMCPMC5706863
OpenAlexW2764181760

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.