Evidence map›Paper›PMID 30115976›Full record

ArticleOncogene2019

KIFC1 regulated by miR-532-3p promotes epithelial-to-mesenchymal transition and metastasis of hepatocellular carcinoma via gankyrin/AKT signaling.

Jihua Han, Fengyue Wang, Yaliang Lan, Jiabei Wang, Chunlei Nie, Yingjian Liang, Ruipeng Song, Tongsen Zheng, Shangha Pan, Tiemin Pei and 13 more

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Integrated Spatial Analysis of Ovarian Precancerous Lesions.bioRxiv : the preprint server for biology · 2025
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  12. High Expression of KIFC1 in Glioma Correlates with Poor Prognosis.Journal of Korean Neurosurgical Society · 2024
    Article
  13. Review
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  18. Article
  19. NFYAv1 is a Tumor-Promoting Transcript Associated with Poor Prognosis of Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2023
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 3 institutions in 1 country.

Jihua HanKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Fengyue WangKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Yaliang LanKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Jiabei WangKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Chunlei NieDepartment of Head and Neck Surgery, The Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Yingjian LiangKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Ruipeng SongKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Tongsen ZhengDepartment of Gastrointestinal Medical Oncology, The Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Shangha PanKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Tiemin PeiKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Changming XieKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Guangchao YangKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Xirui LiuKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Mingxi ZhuKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Yan WangKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Yao LiuKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Fanzheng MengKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Yifeng CuiKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Bo ZhangKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Yufeng LiuKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Xianzhi MengKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. mengxianzhi@sina.com.
Jiewu ZhangDepartment of Head and Neck Surgery, The Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. drzhangjiewu@sohu.com.
Lianxin LiuKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. liulx@ems.hrbmu.edu.cn.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CN

Funding

Changjiang Scholar Program of Chinese Ministry of Education (Changjiang Scholar Program of Ministry of Education of China) No. IRT1122China Postdoctoral Science Foundation 2018M630368National Natural Science Foundation of China (National Science Foundation of China) 81602058National Natural Science Foundation of China (National Science Foundation of China) 8173194National Natural Science Foundation of China (National Science Foundation of China) 81772588
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide. The poor survival may be due to a high proportions of tumor recurrence and metastasis. Kinesin family member C1 (KIFC1) is highly expressed in a variety of neoplasms and is a potential marker for non-small cell lung cancer or ovarian adenocarcinoma metastasis. Nevertheless, the role of KIFC1 in HCC metastasis remains obscure. We investigated this in the present study using HCC cell lines and clinical specimens. Our results indicated that increased levels of KIFC1 were associated with poor prognosis and metastasis in HCC. In addition, KIFC1 induced epithelial-to-mesenchymal transition (EMT) and HCC metastasis both in vitro and in vivo. This tumorigenic effect depended on gankyrin; inhibiting gankyrin activity reversed EMT via activation of protein kinase B (AKT)/Twist family BHLH transcription factor 1 (AKT/TWIST1). We also found that KIFC1 was directly regulated by the microRNA miR-532-3p, whose downregulation was associated with metastatic progression in HCC. These results denote that a decrease in miR-532-3p levels results in increased KIFC1 expression in HCC, leading to metastasis via activation of the gankyrin/AKT/TWIST1 signaling pathway.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorDown-RegulationEpithelial-Mesenchymal TransitionHeterograftsHumansKaplan-Meier EstimateKinesinsLiver NeoplasmsLung NeoplasmsMaleMice, Inbred BALB CMice, NudeMicroRNAsNeoplasm ProteinsAKT1 protein, humanKIFC1 protein, humanKinesinsMicroRNAsMIRN532 microRNA, humanNeoplasm ProteinsNuclear ProteinsProteasome Endopeptidase ComplexProto-Oncogene ProteinsProto-Oncogene Proteins c-aktPSMD10 protein, humanRNA, NeoplasmTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID30115976
PMCPMC6336682
OpenAlexW2887961350

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.