Evidence map›Paper›PMID 32402941›Full record

ArticleMolecular therapy. Nucleic acids2020

Transcriptional Suppression of miR-7 by MTA2 Induces Sp1-Mediated KLK10 Expression and Metastasis of Cervical Cancer.

Chia-Liang Lin, Tsung-Ho Ying, Shun-Fa Yang, Shih-Wei Wang, Shih-Ping Cheng, Jie-Jen Lee, Yi-Hsien Hsieh

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  8. Downregulation of miR‑7 and miR‑153 is involved inInternational journal of oncology · 2023
    Article
  9. Identifying Biomarkers Using Support Vector Machine to Understand the Racial Disparity in Triple-Negative Breast Cancer.Journal of computational biology : a journal of computational molecular cell biology · 2023
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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 5 institutions in 1 country.

Chia-Liang LinInstitute of Biochemistry, Microbiology, and Immunology, Chung Shan Medical University, Taichung, Taiwan; Department of Surgery, MacKay Memorial Hospital and Mackay Medical College, New Taipei City, Taiwan.
Tsung-Ho YingDepartment of Obstetrics and Gynecology, Chung Shan Medical University Hospital, Taichung, Taiwan; Department of Obstetrics and Gynecology, School of Medicine, College of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Shih-Wei WangDepartment of Medicine, Mackay Medical College, New Taipei City, Taiwan; Graduate Institute of Natural Products, College of Pharmacy, Kaohsiung Medical University, Kaohsiung, Taiwan.
Shih-Ping ChengDepartment of Surgery, MacKay Memorial Hospital and Mackay Medical College, New Taipei City, Taiwan; Graduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan; Department of Pharmacology, Taipei Medical University, Taipei, Taiwan.
Jie-Jen LeeDepartment of Surgery, MacKay Memorial Hospital and Mackay Medical College, New Taipei City, Taiwan; Graduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan; Department of Pharmacology, Taipei Medical University, Taipei, Taiwan. Electronic address: jjlee918@mmc.edu.tw.
Yi-Hsien HsiehInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Clinical Laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan. Electronic address: hyhsien@csmu.edu.tw.
Chung Shan Medical University Hospital · TWTaipei Medical University Hospital · TWChung Shan Medical University · TWKaohsiung Medical University · TWMackay Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MTA2 is involved in tumor proliferation and metastasis. However, the role of MTA2 in cervical cancer thus far has not been identified. In this study, we report that elevated expression of MTA2 negatively correlates with Kallikrein-10 (KLK10) expression and poor prognosis of cervical cancer patients. Knockdown of MTA2 substantially inhibited tumor cell migration and invasion, and it enhanced KLK10 expression of the cervical cancer cells in vitro and in vivo. Functionally, shMTA2-mediated suppression of cell mobility was significantly restored by knockdown of KLK10. We also found that Sp1 (transcription factor specificity protein 1) is critical for shMTA2-induced transcriptional upregulation of KLK10 and subsequent biological functions. Furthermore, we found that the expression of miR-7 is elevated by MTA2 silencing and then by direct inhibition of Sp1 expression. Knockdown of Sp1 additively enhanced KLK10 expression in MTA2-knocked down cervical cancer cells, suggesting that the miR-7/Sp1 axis acts as an effector of MTA2 to impact KLK10 levels and mobility of cervical cancer cells. Taken together, our findings provide new insights into the physiological relationship between MTA2 and KLK10 via regulating the miR-7/Sp1 axis, and they provide a potential therapeutic target in cervical cancer.

Indexed as

cervical cancerKLK10miRNA-7MTA2Sp1

Identifiers

PMID32402941
PMCPMC7218230
OpenAlexW3022429962

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.