Evidence map›Paper›PMID 34514691›Full record

ArticleJournal of cellular and molecular medicine2021

Role for calcium-activated potassium channels (BK) in migration control of human hepatocellular carcinoma cells.

Yuan He, Yingying Lin, Fei He, Lijuan Shao, Wei Ma, Fei He

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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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 at 3 institutions in 1 country.

Yuan HeDepartment of General Surgery, Changzhi Medical College Affiliated Heping Hospital, Changzhi, China.
Yingying LinDepartment of Immunology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Fei HeDepartment of Stomatology, The Second Clinical Medical College, Shenzhen People's Hospital, Jinan University, Shenzhen, China.
Lijuan ShaoIntegrated Chinese and Western Medicine Postdoctoral Research Station, Jinan University, Guangzhou, China.
Wei MaTranslational Medicine Collaborative Innovation Center of Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Fei HeTranslational Medicine Collaborative Innovation Center of Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0003-4401-2874
Jinan University · CNChangzhi Medical College · CNFujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. Its high metastasis rate is significantly correlated with poor patient prognosis. Elucidating the molecular mechanism underlying HCC metastasis is essential for HCC treatment. Owing to their high conductance, large-conductance calcium-activated potassium channels (BK channels) play a critical role in the control of membrane potential and have repeatedly been proposed as potential targets for cancer therapy. Emerging evidence suggests that BK channels are involved in the progression of cancer malignancies. The present study investigated the role of BK channels in mediating the hypoxia-stimulated migration of HCC cells both in vitro and in vivo in the absence and presence of various BK channels modulators. We found that BK channels were functionally expressed on the membranes of the SMMC-7721 and Huh7 HCC cell lines. Furthermore, blockage or activation of BK channels on the surface of HCC cells correspondingly inhibited or promoted HCC cell proliferation, migration and invasion in hypoxia conditions, with altered expression and distribution of cell-cell adhesion molecule E-cadherin and typical marker of mesenchymal cells, Vimentin, but not N-cadherin. Hypoxia conditions did not alter BK channels expression but increased its open probability. Moreover, BK channels blocker IbTX significantly inhibited HCC cell remote colonization in HCC cell xenografted mice. In conclusion, the results of this study suggest that blocking BK channels offers an attractive strategy for treating HCC.

Indexed as

AnimalsCarcinoma, HepatocellularCell CycleCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalElectrophysiological PhenomenaHeterograftsHumansIon Channel GatingLiver NeoplasmsMicePotassium Channel BlockersPotassium Channels, Calcium-ActivatedXenograft Model Antitumor AssaysPotassium Channel BlockersPotassium Channels, Calcium-ActivatedBK channelshepatocellular carcinomamigrationproliferationxenografted mice

Identifiers

PMID34514691
PMCPMC8505838
OpenAlexW3199395467

What Socratic 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 Socratic graph.