Evidence map›Paper›PMID 34887379›Full record

ArticleCell death discovery2021

SPTBN2 regulated by miR-424-5p promotes endometrial cancer progression via CLDN4/PI3K/AKT axis.

Pengling Wang, Ting Liu, Zhendan Zhao, Zhiling Wang, Shujie Liu, Xingsheng Yang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Role of miR-424 in the carcinogenesis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. miR-424(322)-5p targetsActa biochimica et biophysica Sinica · 2023
    Article
  12. Claudin-4: A New Molecular Target for Epithelial Cancer Therapy.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. A Bioinformatics Study of Immune Infiltration-Associated Genes in Sciatica.Computational intelligence and neuroscience · 2022
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Pengling WangDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, People's Republic of China.
Ting LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, People's Republic of China.
Zhendan ZhaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, People's Republic of China.
Zhiling WangDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, People's Republic of China.
Shujie LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, People's Republic of China.
Xingsheng YangDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, People's Republic of China. xingshengyang@sdu.edu.cn.ORCID http://orcid.org/0000-0002-4946-2033
Qilu Hospital of Shandong University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81874105
6 · The paper itself

Abstract

Endometrioid Endometrial Cancer (EEC) is the main subtype of endometrial cancer. In our study, we demonstrated that SPTBN2 was significantly overexpressed in EEC tissues. Upregulated SPTBN2 expression was positively associated with poor prognosis. In addition, we testified that SPTBN2 knockdown significantly inhibited the proliferation, migration, and invasion of EEC cells. Moreover, we found SPTBN2 could interact with CLDN4 to promote endometrial cancer metastasis via PI3K/AKT pathway. Then we further demonstrated that CLDN4 is upregulated in EEC and promotes EEC metastasis. CLDN4 overexpression could partially reversed the decrease in cell migration and invasion caused by SPTBN2 downregulation. In addition, we confirmed that SPTBN2 was a target of miR-424-5p, which plays a tumor suppressor in endometrial cancer. Rescue experiments showed that inhibition of SPTBN2 could partially reverse the effect of miR-424-5p in EEC. In conclusion, we demonstrated that by acting as a significant target of miR-424-5p, SPTBN2 could interact with CLDN4 to promote endometrial cancer metastasis via PI3K/AKT pathway in EEC. Our study revealed the prognostic and metastatic effects of SPTBN2 in EEC, suggesting that SPTBN2 could serve as a prognostic biomarker and a target for metastasis therapy.

Identifiers

PMID34887379
PMCPMC8660803
OpenAlexW4200389215

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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 OpenQuestion graph.