Evidence map›Paper›PMID 28319061›Full record

ArticleOncogene2017

CCDC178 promotes hepatocellular carcinoma metastasis through modulation of anoikis.

X Hu, Y Zhao, L Wei, B Zhu, D Song, J Wang, L Yu, J Wu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  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

8 authors at 4 institutions in 1 country.

X HuThe State Key Laboratory of Genetic Engineering, Zhongshan Hospital and School of Life Science, Fudan University, Shanghai, People's Republic of China.
Y ZhaoThe State Key Laboratory of Genetic Engineering, Zhongshan Hospital and School of Life Science, Fudan University, Shanghai, People's Republic of China.
L WeiDepartment of Oncology, The 401 Hospital of PLA, Qingdao, People's Republic of China.
B ZhuThe State Key Laboratory of Genetic Engineering, Zhongshan Hospital and School of Life Science, Fudan University, Shanghai, People's Republic of China.
D SongThe State Key Laboratory of Genetic Engineering, Zhongshan Hospital and School of Life Science, Fudan University, Shanghai, People's Republic of China.
J WangThe State Key Laboratory of Genetic Engineering, Zhongshan Hospital and School of Life Science, Fudan University, Shanghai, People's Republic of China.
L YuThe State Key Laboratory of Genetic Engineering, Zhongshan Hospital and School of Life Science, Fudan University, Shanghai, People's Republic of China.
J WuThe State Key Laboratory of Genetic Engineering, Zhongshan Hospital and School of Life Science, Fudan University, Shanghai, People's Republic of China.
Zhongshan Hospital · CNFudan University · CNState Key Laboratory of Genetic EngineeringPeople's Liberation Army 401 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most malignant tumors with high rate of recurrence and metastasis. Coiled-coil domain-containing protein 178 (CCDC178) has been reported to be mutated in HCC, whereas its role in physiological and pathologic process, including in human cancer, remains largely unknown. Here, we found that CCDC178 is upregulated in HCC tissues and its overexpression is correlated with pathological stage (P=0.003). CCDC178 deficiency reduced the anchorage-independent growth and anoikis resistance of HCC cells, and inhibited the HCC metastasis in vivo. Mechanistically, CCDC178 associated with BRCA1-associated protein 2 (BRAP2), a negative regulator of extracellular signal-regulated kinase (ERK) pathway, and promoted its degradation. Moreover, CCDC178 deficiency impaired the ERK activation, which is dependent on BRAP2. In conclusion, we identify CCDC178 as a novel candidate oncogene involved in anoikis resistance and HCC metastasis, and raise the possibility that CCDC178 may be a new therapeutic target for HCC.

Indexed as

AdultAgedAged, 80 and overAnimalsAnoikisCarcinoma, HepatocellularCell AdhesionCell Line, TumorCell MovementCytoskeletal ProteinsFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansLiver NeoplasmsMaleCCDC178 protein, humanCytoskeletal Proteins

Identifiers

PMID28319061
OpenAlexW2602917813

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.