Evidence map›Paper›PMID 27478331›Full record

ArticleJournal of Korean medical science2016

OTX1 Contributes to Hepatocellular Carcinoma Progression by Regulation of ERK/MAPK Pathway.

Hua Li, Qian Miao, Chun-Wei Xu, Jian-Hui Huang, Yue-Fen Zhou, Mei-Juan Wu

Abstract read
In one paragraph

Article in Journal of Korean medical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. International journal of molecular sciences · 2023
    Review
  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. Article
  19. Article
  20. 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

6 authors.

Hua LiDepartment of Anesthesiology, Shanghai Pulmonary Hospital, Tongji University, School of Medicine, Shanghai, China .ORCID 0000-0003-1728-1622
Qian MiaoDepartment of Oncology, Quzhou People's Hospital in Zhejiang Province, Quzhou Zhejiang, China .ORCID 0000-0002-1864-5697
Chun-Wei XuDepartment of Pathology, Affiliated Hospital Cancer Center, Academy of Military Medical Sciences, Beijing, China .ORCID 0000-0002-9021-6731
Jian-Hui HuangDepartment of Oncology, Lishui Central Hospital, Lishui Hospital of Zhejiang University, Lishui, Zhejiang, China .ORCID 0000-0002-2854-112X
Yue-Fen ZhouDepartment of Oncology, Lishui Central Hospital, Lishui Hospital of Zhejiang University, Lishui, Zhejiang, China .ORCID 0000-0002-0872-9782
Mei-Juan WuDepartment of Pathology, Zhejiang Cancer Hospital, Hangzhou Zhejiang, China .ORCID 0000-0001-7893-2287

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Orthodenticlehomeobox 1 (OTX1) overexpression had previously been associated with the progression of several tumors. The present study aimed to determine the expression and role of OTX1 in human hepatocellular carcinoma (HCC). The expression level of OTX1 was examined by quantitative real-time PCR (qRT-PCR) in 10 samples of HCC and paired adjacent non-cancerous tissues, and by immunohistochemistry (IHC) analysis in 128 HCC samples and matched controls. The relationship between OTX1 expression and the clinicopathological features werealso analyzed. Furthermore, the effects of OTX1 knockdown on cell proliferation and migration were determined in HCC cell lines. Axenograft mouse model was also established to investigate the role of OTX1 in HCC tumor growth. TheqRT-PCR and IHC analyses revealed that OTX1 was significantly elevated in HCC tissues compared with the paired non-cancerous controls. Expression of OTX1 was positively correlated with nodal metastasis status (P = 0.009) and TNM staging (P = 0.001) in HCC tissues. In addition, knockdown of OTX1 by shRNA significantly inhibited the proliferation and migration, and induced cell cycle arrest in S phase in vitro. Tumor growth was markedly inhibited by OTX1 silencing in the xenograft. Moreover, OTX1 silencing was causable for the decreased phosphorylation level of ERK/MAPK signaling. In conclusion, OTX1 contributes to HCC progression possibly by regulation of ERK/MAPK pathway. OTX1 may be a novel target for molecular therapy towards HCC.

Indexed as

AgedAnimalsBlotting, WesternCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryLiverLiver NeoplasmsLymphatic MetastasisMaleOTX1 protein, humanOtx Transcription FactorsERK/MAPKGrowthHepatocellular CarcinomaMigrationOTX1

Identifiers

PMID27478331
PMCPMC4951550

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.