Evidence map›Paper›PMID 36348252›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2023

FUT8 is regulated by miR-122-5p and promotes malignancies in intrahepatic cholangiocarcinoma via PI3K/AKT signaling.

Fanghua Chen, Yin Li, Ling Aye, Yingcheng Wu, Liangqing Dong, Zijian Yang, Qiang Gao, Shu Zhang

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. iScience · 2023
    Article
  10. Core fucosylation and its roles in gastrointestinal glycoimmunology.World journal of gastrointestinal oncology · 2023
    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

8 authors at 3 institutions in 1 country.

Fanghua ChenLiver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, 200032, China.
Yin LiDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Ling AyeDepartment of Otolaryngology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Yingcheng WuLiver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, 200032, China.
Liangqing DongLiver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, 200032, China.
Zijian YangLiver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, 200032, China.
Qiang GaoLiver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, 200032, China.
Shu ZhangLiver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, 200032, China. zhang.shu@zs-hospital.sh.cn.
Fudan University · CNZhongshan Hospital · CNEye & ENT Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntrahepatic cholangiocarcinoma (iCCA) is the second-most lethal primary liver cancer and its prognosis remains dismal. N-glycosylation, which is biosynthesized by a number of glycosyltransferases, plays an important role in a variety of biological processes and is associated with cancer development and progression.

methodsBased on our previous proteogenomic resources from an iCCA cohort of 262 patients, fucosyltransferases 8 (FUT8) showed significant prognosis relevance in iCCA. Tumor tissues from iCCA patients were used to evaluate the correlation between its expression and clinical information. Gain/loss-of-function experiments in iCCA cell lines were performed to elucidate the biological function of FUT8. In addition, its downstream pathways and post-transcriptional regulators were inferred and verified.

resultsElevated FUT8 expression was clinically associated with worse overall survival in iCCA patients. Its overexpression promoted migration, invasion and proliferation ability of iCCA cells. In addition, miR-122-5p was found to act as a post-transcriptional regulator of FUT8 and proved to inhibit FUT8 expression and then suppress the proliferation and migration ability of iCCA cell lines. Furthermore, FUT8 was observed to promote iCCA development through PI3K/AKT signaling pathway.

conclusionsThese findings demonstrated that FUT8, regulated by miR-122-5p, could be a tumor promoter of iCCA through PI3K/AKT signaling pathway.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaMicroRNAsBile Ducts, IntrahepaticCell Line, TumorCell ProliferationHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionMicroRNAsMIRN122 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktFUT8Intrahepatic cholangiocarcinomamiR-122-5pPI3K/AKT signaling pathway

Identifiers

PMID36348252
PMCPMC12974632
OpenAlexW4308532276

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.