Evidence map›Paper›PMID 31736268›Full record

ArticleJournal of cellular and molecular medicine2020

LncRNA SPRY4-IT1 regulates breast cancer cell stemness through competitively binding miR-6882-3p with TCF7L2.

Xinyue Song, Xiaoxue Zhang, Xinnan Wang, Lianze Chen, Longyang Jiang, Ang Zheng, Ming Zhang, Lin Zhao, Minjie Wei

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Long non-coding RNAs: Key regulators of stemness in breast cancer.Frontiers in cell and developmental biology · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Long non-coding RNAs in breast cancer stem cells.Medical oncology (Northwood, London, England) · 2023
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Network Pharmacology Analysis, Molecular Docking, andEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  20. 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

9 authors at 2 institutions in 1 country.

Xinyue SongDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.ORCID 0000-0002-6831-9750
Xiaoxue ZhangDepartment of Medical Imaging, Cancer Hospital of China Medical University, Shenyang, China.
Xinnan WangDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Lianze ChenDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Longyang JiangDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Ang ZhengDepartment of Breast Surgery, The First Affiliated Hospital of China Medical University, Shenyang, China.
Ming ZhangDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Lin ZhaoDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Minjie WeiDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.ORCID 0000-0002-0404-7098
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SPRY4-intronic transcript 1 has been found in several kinds of cancers, but the role of SPRY4-IT1 in breast cancer stem cells has not been studied. We investigated whether SPRY4-IT1 is involved in the promotion of breast cancer stem cells (BCSCs). We used qRT-PCR to detect the expression of SPRY4-IT1 in MCF-7 cells and MCF-7 cancer stem cells (MCF-7 CSCs). The effects of SPRY4-IT1 on the proliferation and renewal ability of breast cancer cells were investigated by in vitro and in vivo assays (ie in situ hybridization, colony formation assay, sphere formation assay, flow cytometry assay, western blotting, xenograft model and immunohistochemistry). The mechanism of SPPRY4-IT1 as a ceRNA was studied by a dual-luciferase reporter assay and bioinformatic analysis. In our study, SPRY4-IT1 was up-regulated in MCF-7 CSCs compared with MCF-7 cells, and high SPRY4-IT1 expression was related to reduced breast cancer patient survival. Furthermore, SPRY4-IT1 overexpression promoted breast cancer cell proliferation and stemness in vitro and in vivo. In addition, SPRY4-IT1 knockdown suppressed BCSC renewal ability and stemness maintenance in vivo and in vitro. The dual-luciferase reporter assays indicated that SPRY4-IT1 as a sponge for miR-6882-3p repressed transcription factor 7-like 2 (TCF7L2) expression. Taken together, these findings demonstrated that SPRY4-IT1 promotes proliferation and stemness of breast cancer cells as well as renewal ability and stemness maintenance of BCSCs by increasing the expression of TCF7L2 through targeting miR-6882-3p.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorBreast NeoplasmsCell ProliferationFemaleHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsNeoplastic Stem CellsRNA, Long NoncodingTranscription Factor 7-Like 2 ProteinTumor Cells, CulturedBiomarkers, Tumorlong noncoding RNA SPRY4-IT1, humanMicroRNAsRNA, Long NoncodingTCF7L2 protein, humanTranscription Factor 7-Like 2 Proteinbreast cancermiR-6882-3pSPRY4-IT1stem cellsTCF7L2

Identifiers

PMID31736268
PMCPMC6933354
OpenAlexW2982957921

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.