Evidence map›Paper›PMID 39917006›Full record

ArticleCytoJournal2024

Preliminary study on the cellular and molecular mechanisms of Cms1 ribosomal small subunit homolog promoting hepatocellular carcinoma progression via activation of the homolog family member A/yes-associated protein 1 signaling pathway.

Yao Zheng, Aiyun Wang, Shuaijun Yu, Benzun Wei, Xiao Lyu

Abstract read
In one paragraph

Article in CytoJournal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025
    Review
  2. 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

5 authors.

Yao ZhengDepartment of Pathology, Zibo Central Hospital, Zibo City, Shandong Province, China.
Aiyun WangDepartment of Pathology, Zibo Municipal Hospital, Zibo City, Shandong Province, China.
Shuaijun YuDepartment of Intensive Care Medicine, Huantai County Traditional Chinese Medicine Hospital, Zibo City, Shandong Province, China.
Benzun WeiDepartment of Hepatobiliary Surgery, Zibo Central Hospital, Zibo City, Shandong Province, China.
Xiao LyuDepartment of Medical Oncology, Zibo Central Hospital, Zibo City, Shandong Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: The precise mechanism of action of cms1 ribosomal small subunit homolog (CMSS1) in hepatocellular carcinoma (HCC) is yet unknown, although it may be essential to the malignant evolution of disease. The aim of this study was to reveal the role of CMSS1 in HCC and its possible mechanism. Material and Methods: The expression of CMSS1 in different HCC cell lines was detected by quantitative real-time polymerase chain reaction and Western blot. The expression of CMSS1 in HCC cells was subsequently silenced, and the proliferation capacity of HCC cells was measured by colony formation assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, and flow cytometry, and the migration and metastasis capacity of the HCC cells was measured by Transwell assay and Western blot. Finally, ras homolog family member A (RhoA) and yes-associated protein 1 (YAP1) were silenced, and the relationship between CMSS1, RhoA, and YAP1 was further discussed by immunofluorescence, colony formation assay, and EdU assay. Results: The experimental results showed that CMSS1 is highly expressed in HCC tissues and cell lines ( Conclusion: CMSS1 promotes the malignant progression of HCC by activating the RhoA GTPase/YAP1 signaling pathway.

Indexed as

Cms1 ribosomal small subunit homologEs-associated protein 1Hepatocellular carcinomaMalignant progressionRas homolog family member A GTPase

Identifiers

PMID39917006
PMCPMC11801666

What Socratic holds

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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 Socratic graph.