Evidence map›Paper›PMID 38067506›Full record

ArticleMolecules (Basel, Switzerland)2023

Silencing LY6D Expression Inhibits Colon Cancer in Xenograft Mice and Regulates Colon Cancer Stem Cells' Proliferation, Stemness, Invasion, and Apoptosis via the MAPK Pathway.

Jinyue Duan, Yi Wang, Yuanyuan Chen, Yujue Wang, Qisen Li, Jinrui Liu, Changhao Fu, Chenyu Cao, Zhongyi Cong, Manman Su

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

8 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Silencing LY6K Suppresses CD44Current issues in molecular biology · 2024
    Article
  7. Article
  8. Article
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

10 authors at 2 institutions in 2 countries.

Jinyue DuanDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Yi WangDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.ORCID 0000-0003-4021-1067
Yuanyuan ChenDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Yujue WangDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Qisen LiDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Jinrui LiuDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Changhao FuVA Palo Alto Health Care System, Medical School, Stanford University, Palo Alto, CA 94304, USA.ORCID 0000-0001-7568-3369
Chenyu CaoDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Zhongyi CongDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.ORCID 0000-0001-8020-3921
Manman SuDepartment of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.ORCID 0000-0002-4664-8940
Jilin University · CNVA Palo Alto Health Care System · US

Funding

Graduate Innovation Fund of Jilin University 2023CX242Jilin Province Science and Technology Department 20220204022YY
6 · The paper itself

Abstract

This study explored the role of lymphocyte antigen 6 family member D (LY6D) in colon cancer stem cells' (CCSCs) proliferation and invasion. LY6D was knocked down using siRNA, and the down-regulation of LY6D was verified using Western blotting. After LY6D knockdown, CCSCs' proliferation, stemness, and invasion were suppressed, whereas apoptosis was increased. Gene Ontology (GO) enrichment analysis revealed that the differentially expressed genes (DEGs) between siLY6D and the negative control groups were significantly enriched in the cell-substrate adherens junction, focal adhesion, and cell-substrate junction terms. Meanwhile, the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that the DEGs were significantly enriched in the MAPK pathway. In addition, Western blotting results showed that pBRAF and pERK1/2, cascade kinases of the MAPK pathway, were significantly down-regulated after LY6D knockdown. In addition, nude mice xenograft experiments showed that the siLY6D treatment decreased tumor sizes and weights and improved tumor-bearing mice survival rates compared with the control group. In conclusion, these findings indicate that LY6D, which is highly expressed in CCSCs, is a key factor involved in tumor growth and development and might be a potential cancer marker and therapeutic target for colon cancer.

Indexed as

Colonic NeoplasmsAnimalsApoptosisCell Adhesion MoleculesCell ProliferationGene Expression Regulation, NeoplasticGPI-Linked ProteinsHeterograftsHumansMiceMice, NudeNeoplastic ProcessesNeoplastic Stem CellsCell Adhesion MoleculesGPI-Linked ProteinsLY6D protein, humancancer stem cellscolon cancerLY6DMAPK

Identifiers

PMID38067506
PMCPMC10708431
OpenAlexW4389056092

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.