Evidence map›Paper›PMID 35425722›Full record

ArticleJournal of hepatocellular carcinoma2022

MCT4 Promotes Hepatocellular Carcinoma Progression by Upregulating TRAPPC5 Gene.

Zheyu Niu, Faji Yang, Hongguang Li, Jianlu Wang, Qingqiang Ni, Chaoqun Ma, Huaqiang Zhu, Hong Chang, Xu Zhou, Jun Lu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of hepatocellular carcinoma, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

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  11. Role of lactate and lactate metabolism in liver diseases (Review).International journal of molecular medicine · 2024
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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

11 authors at 2 institutions in 1 country.

Zheyu Niu *Department of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Faji Yang *Department of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Hongguang Li *Department of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Jianlu WangDepartment of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Qingqiang NiDepartment of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Chaoqun MaDepartment of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Huaqiang ZhuDepartment of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Hong ChangDepartment of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Xu ZhouDepartment of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Jun LuDepartment of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Hengjun GaoDepartment of Hepatobiliary Surgery, Shandong Provincial Hospital, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, People's Republic of China.
Shandong University · CNShandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Monocarboxylate transporter 4 (MCT4) is an important component of cancer cell glycolytic metabolism. It has been confirmed that MCT4 is highly expressed in hepatocellular carcinoma (HCC) cells and tissues and is significantly associated with poor prognosis of HCC patients. However, research on its downstream molecules that affect HCC is still insufficient. The aim of current research was to investigate the MCT downstream molecule and its role of in HCC development. Patients and Methods: After MCT4 expression was knocked down by RNA interference, RNA sequencing and quantitative real-time PCR were used to screen for differentially expressed genes in an HCC cell line (HCCLM3). Immunohistochemistry in HCC tissue microarray was carried out to evaluate the Trafficking Protein Particle Complex Subunit 5 (TRAPPC5) expression. Cell proliferation, migration, and invasion were evaluated by CCK-8 assay, colony formation assay, transwell and wound-healing test, respectively. Xenograft experiment was employed to investigate the function of TRAPPC5 on tumor growth in vivo. Related signaling pathway proteins were evaluated by Western blot. Results: TRAPPC5 expression was significantly downregulated after knocking down of MCT4 in HCCLM3. TRAPPC5 was highly expressed in HCC tissues, and it could enhance the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process of HCC cells. In vivo experiment showed that TRAPPC5 could promote HCC tumorigenesis. Conclusion: In the process of MCT4 affecting the progression of HCC, TRAPPC5 is one of the most important related molecules. TRAPPC5 suppression could significantly reduce HCC cell proliferation, migration and invasion and could serve as a therapeutic target in HCC.

Indexed as

hepatocellular carcinomaMCT4RNA sequencingtissue microarraysTRAPPC5

Identifiers

PMID35425722
PMCPMC9005128
OpenAlexW4225698724

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.