Evidence map›Paper›PMID 39737000›Full record

ArticleFrontiers in genetics2024

miR-210 loss leads to widespread phenotypic and gene expression changes in human 293T cells.

Xiaoxiao Zhang, Zhen Meng, Chengyong Yang, Chenghao Wang, Kexin Zhang, Anxin Shi, Jingjing Guo, Yong Feng, Yan Zeng

Abstract read
In one paragraph

Article in Frontiers in genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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.

Xiaoxiao ZhangDepartment of Zoology, College of Life Sciences, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Zhen MengDepartment of Zoology, College of Life Sciences, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Chengyong YangDepartment of Zoology, College of Life Sciences, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Chenghao WangDepartment of Zoology, College of Life Sciences, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Kexin ZhangDepartment of Zoology, College of Life Sciences, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Anxin ShiDepartment of Zoology, College of Life Sciences, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Jingjing GuoCentre in Artificial Intelligence Driven Drug Discovery, Faculty of Applied Sciences, Macao Polytechnic University, Macao, China.
Yong FengInstitute of Medical Virology, School of Basic Medical Sciences, Wuhan University, Wuhan, Hubei, China.
Yan ZengDepartment of Zoology, College of Life Sciences, Nanjing Agricultural University, Nanjing, Jiangsu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Hypoxia responses are critical for myriad physiological and pathological processes, such as development, tissue repair, would healing, and tumorigenesis. microRNAs (miRNAs) are a class of small non-coding RNAs that exert their functions by inhibiting the expression of their target genes, and miR-210 is the miRNA universally and most conspicuously upregulated by hypoxia in mammalian systems. For its relationship to hypoxia, miR-210 has been studied extensively, yet no consensus exists on the roles and mechanisms of miR-210 in human physiological processes or diseases, and we know little about genuine miR-210 target genes in humans. Methods: To better investigate the functions and mechanisms of human miR-210, therefore, we derived the human Results and Discussion: We found that the loss of miR-210 altered a variety of cellular phenotypes including proliferation and apoptosis. Subsequent global gene expression analyses identified plausible mechanisms underlying these phenotypic changes in 293T cells. In particular, we showed that miR-210 might target the expression of BNIP3L as a potential mechanism to suppress apoptosis. Surprisingly, the mRNA levels of most previously reported miR-210 target genes were not induced upon

Indexed as

apoptosisBnip3LCRISPR/Cas9miR-210target gene

Identifiers

PMID39737000
PMCPMC11683127

What Socratic holds

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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 Socratic graph.