Evidence map›Paper›PMID 35422067›Full record

ArticleCell death discovery2022

SNORD1C maintains stemness and 5-FU resistance by activation of Wnt signaling pathway in colorectal cancer.

Yonghui Liu, Chengwen Zhao, Guihua Wang, Jing Chen, Shaoqing Ju, Jianfei Huang, Xudong Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Translational cancer research · 2025
    Article
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  10. Small nucleolar RNAs: the hidden precursors of cancer ribosomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
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  13. Article
  14. SnoRNAs: The promising targets for anti-tumor therapy.Journal of pharmaceutical analysis · 2024
    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

7 authors at 1 institution in 1 country.

Yonghui Liu *Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Chengwen Zhao *Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Guihua WangDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Jing ChenDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Shaoqing JuDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Jianfei HuangDepartment of Clinical Biobank, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Xudong WangDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China. wangxudong88@hotmail.com.ORCID http://orcid.org/0000-0002-3522-3971
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small nucleolar RNAs (snoRNAs) are a class of non-coding RNAs that play indispensable roles in cancers, including colorectal cancer (CRC). However, the role of SNORD1C in CRC is unclear. In the current study, SNORD1C expression was measured in CRC tissues using quantitative real-time PCR. A series of in vivo and in vitro experiments were performed to examine the functional role of SNORD1C in CRC. Quantitative real-time PCR, western blotting, sphere formation assay, and chemotherapy resistance analysis were conducted to illustrate the SNORD1C molecular mechanism. SNORD1C was upregulated in CRC and that high SNORD1C expression was related to poor prognosis. After knocking down SNORD1C in CRC cell lines, cell proliferation, colony formation, cell migration, and invasion were alleviated, while apoptosis was increased. Transcriptional RNA-sequencing analysis revealed that following SNORD1C knockdown, β-catenin was downregulated, as was the transcription factor TCF7, which inhibited the Wnt/β-catenin pathway. Meanwhile, levels of the stem cell-related factors were reduced, diminishing cell stemness and tumorigenesis. Our findings suggest that SNORD1C functions via the Wnt/β-catenin pathway to enhance cancer cell stemness in CRC and could be a predictive biomarker for the prognosis ad aggressiveness of this malignancy. Additionally, targeting SNORD1C may be a novel therapeutic strategy for CRC.

Identifiers

PMID35422067
PMCPMC9010412
OpenAlexW4223894585

What OpenQuestion 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 OpenQuestion graph.