Evidence map›Paper›PMID 33727860›Full record

ArticleCancer management and research2021

Knockdown of SLC39A4 Expression Inhibits the Proliferation and Motility of Gallbladder Cancer Cells and Tumor Formation in Nude Mice.

Min Li, Kun Fan, Bohao Zheng, David Zekria, Tao Suo, Han Liu, Sheng Shen, Houbao Liu, Xiaoling Ni

Open access · goldAbstract read
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Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

Min Li *Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.ORCID 0000-0003-4026-0440
Kun Fan *Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Bohao Zheng *Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.ORCID 0000-0003-0934-8209
David ZekriaDepartment of Radiology, Leicester Royal Infirmary, Leicester, LE1 5WW, UK.
Tao SuoDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Han LiuDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Sheng ShenDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Houbao LiuDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Xiaoling NiDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Sun Yat-sen University · CNLeicester Royal Infirmary · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGallbladder cancer (GBC) is a common malignancy of the biliary tract and is characterized by rapid progression and early metastasis. Elucidating the molecular mechanisms of GBC could help to develop better treatment strategies. MATERIALS AND

methodsHuman GBC cell lines (GBC-SD and NOZ) were applied to determine the capacity of the proliferation and migration of cells using the MTT assay, colony formation, wound-healing assay as well as the Transwell™ assay. A nude xenograft was used to evaluate tumor growth in vivo.

resultsUsing two types of GBC cell lines, we found that absence of solute carrier family (SLC) 39A4 (which encodes the zinc transporter ZRT/IRT-like protein [ZIP]4), could suppress the proliferation and migration of cells. Additionally, absence of ZIP4 could impair growth of xenografts in nude mice. While, over-expression of SLC39A4 could promote the GBC cell proliferation and migration, and inhibit apoptosis. We revealed that SLC39A4 might affect GBC progression by modulating the signaling pathways responsible for the survival, energy supply and metastasis of cells, and indicated that SLC39A4 could serve as a novel therapeutic target for GBC.

conclusionSLC39A4 promoted the viability and motility of GBC cells, and tumor formation in nude mice. We demonstrated an oncogenic potential for SLC39A4.

Indexed as

gallbladder cancermigrationpotential therapeutic targetproliferationSLC39A4 (ZIP4)

Identifiers

PMID33727860
PMCPMC7955045
OpenAlexW3135186743

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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.