Evidence map›Paper›PMID 32860308›Full record

ArticleCancer science2020

Suppressor of Ty 16 promotes lung cancer malignancy and is negatively regulated by miR-1227-5p.

Lu Yang, Xing Wang, Xinyan Jiao, Bixia Tian, Miao Zhang, Can Zhou, Ruiqi Wang, He Chen, Bo Wang, Juan Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  4. Silencing ofInsects · 2022
    Article
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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

13 authors at 1 institution in 1 country.

Lu YangCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.ORCID https://orcid.org/0000-0002-2982-990X
Xing WangDepartment of Pathology, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Xinyan JiaoCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Bixia TianCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.ORCID https://orcid.org/0000-0002-2390-7022
Miao ZhangCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Can ZhouDepartment of Breast Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Ruiqi WangCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
He ChenCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Bo WangCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Juan LiCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Jie LiuCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Guanjun ZhangDepartment of Pathology, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Peijun LiuCenter for Translational Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.ORCID https://orcid.org/0000-0002-0767-0774
First Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

National Natural Science Foundation of China 81872272
6 · The paper itself

Abstract

Suppressor of Ty 16 (Spt16) is a component of the facilitates chromatin transcription (FACT) complex, which is a histone chaperone and involved in gene transcription, DNA replication, and DNA repair. Previous studies showed that FACT is highly expressed in cancer, and cancer cells are more reliant on FACT than normal cells. However, the relationship between Spt16 and lung cancer remains unclear. In this study, we explored the functions of Spt16 in lung cancer cells. The effects of Spt16 on lung cancer cell proliferation, cell cycle progression, apoptosis, migration, and invasion were examined. We found that knockdown of Spt16 led to obvious decreases of both Rb and MCM7, and further activated the DNA damage response (DDR) pathway. In addition, a novel micro-RNA, miR-1227-5p, directly targeted the 3'-UTR of Spt16 and regulated the mRNA levels of Spt16. Furthermore, we found that CBL0137, the functional inhibitor of FACT, showed similar effects as loss of Spt16. Together, our data indicated that Spt16 is likely to be an essential regulator for lung cancer malignancy and is negatively regulated by miR-1227-5p.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsApoptosisCarbazolesCell CycleCell Cycle ProteinsChromatinDisease ProgressionDNA DamageGene Knockdown TechniquesHumansLung NeoplasmsMicroRNAsNeoplasm GradingRNA InterferenceTranscription Factors3' Untranslated RegionsCarbazolesCBLC137Cell Cycle ProteinsChromatinMicroRNAsSUPT16H protein, humanTranscription Factorslung cancerMCM7MiR-1227-5pRbSpt16

Identifiers

PMID32860308
PMCPMC7648015
OpenAlexW3082243924

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.