Evidence map›Paper›PMID 38736729›Full record

ArticleCytotechnology2024

LncRNA MIR181A2HG negatively regulates human keratinocytes proliferation by binding SRSF1.

Xiaomei Fan, Mingzhao Li, Mutian Niu, Fangru Chen, Zhijing Mo, Pengpeng Yue, Mengjiao Wang, Qingbo Liu, Bin Liang, Shaoqin Gan and 2 more

Abstract read
In one paragraph

Article in Cytotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. 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

12 authors.

Xiaomei Fan *School of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Mingzhao Li *School of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Mutian NiuSchool of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Fangru ChenDepartment of Dermatology, Affiliated Hospital of Guilin Medical University, Guilin, 541001 Guangxi People's Republic of China.
Zhijing MoSchool of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Pengpeng YueSchool of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Mengjiao WangDepartment of Dermatology, Affiliated Hospital of Guilin Medical University, Guilin, 541001 Guangxi People's Republic of China.
Qingbo LiuSchool of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Bin LiangSchool of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Shaoqin GanSchool of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Chengke WengSchool of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.
Jintao GaoSchool of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, 541199 Guangxi People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a common chronic inflammatory skin disease. Abnormal proliferation of keratinocytes plays an important role in the pathogenesis of psoriasis. Long non-coding RNAs (lncRNAs) are involved in the regulation of a variety of cell biological processes. The purpose of this study was to investigate the potential role of lncRNA MIR181A2HG in the proliferation of human keratinocytes. qRT-PCR and Western blotting were performed to measure the expression levels of MIR181A2HG, SRSF1, KRT6, and KRT16 in tissue specimens and HaCaT keratinocytes. The effects of MIR181A2HG on HaCaT keratinocytes proliferation were evaluated using Cell Counting Kit-8 (CCK-8) assays, 5-Ethynyl-2'-deoxyuridine (EdU) incorporation, and cell-cycle assays. RNA pulldown-mass spectrometry (MS) was applied to identify the proteins interacting with MIR181A2HG. RNA pull-down-Western blotting and RNA immunoprecipitation coupled with real-time quantitative reverse transcription-PCR (RIP-qRT-PCR) assays were used to determine the interactions between MIR181A2HG and its RNA-binding proteins (RBPs). MIR181A2HG was down-regulated in psoriasis tissues. MIR181A2HG overexpression induced G0/G1 and G2/M phase cell cycle arrest and decreased the protein levels of KRT6, KRT16, Cyclin D1, CDK4, and Cyclin A2 in HaCaT keratinocytes. MIR181A2HG knockdown showed the opposite effect. By using RNA pulldown-MS, 356 proteins were identified to interact with MIR181A2HG potentially. Bioinformatics analysis showed that NOP56 and SRSF1 may be RNA binding proteins (RBPs) that may be interact with MIR181A2HG. Furthermore, by using RNA pull-down-Western blotting and RIP-qRT-PCR, SRSF1 was determined to interact with MIR181A2HG. Moreover, silencing of SRSF1 inhibited keratinocytes proliferation, which could be reversed with the knockdown of MIR181A2HG. Our findings indicated that MIR181A2HG can negatively regulate HaCaT keratinocytes proliferation by binding SRSF1, suggesting that MIR181A2HG and SRSF1 may serve as potential targets for the treatment of psoriasis. Supplementary Information: The online version contains supplementary material available at 10.1007/s10616-024-00621-6.

Indexed as

KeratinocytesLncRNAsMIR181A2HGProliferationPsoriasisSRSF1

Identifiers

PMID38736729
PMCPMC11082102

What Socratic holds

Textmetadata
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 Socratic graph.