Evidence map›Paper›PMID 31933969›Full record

ArticleInternational journal of clinical and experimental pathology2019

MicroRNA-221 inhibits human papillomavirus 16 E1-E2 mediated DNA replication through activating SOCS1/Type I IFN signaling pathway.

Haikong Lu, Xin Gu

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. RSF1 in cancer: interactions and functions.Cancer cell international · 2021
    Review
  13. Article
  14. 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

2 authors at 1 institution in 1 country.

Haikong LuDepartment of Sexually Transmitted Disease Institute, Shanghai Skin Disease Hospital Shanghai 200050, China.
Xin GuDepartment of Sexually Transmitted Disease Institute, Shanghai Skin Disease Hospital Shanghai 200050, China.
Shanghai Skin Disease Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human Papillomavirus (HPV) 16 infection has led to clinical disorders and is considered one of the important causes of human cervical cancer. Recently, microRNAs (miRNAs) have been proven to play an important role in many viral infections through regulating the Type I IFN immune response. However, reports concerning the role of miRNAs in HPV 16 infection are unclear. The aim of this study was to identify and evaluate the potential functions of miRNAs in HPV 16 replication and reveal the detailed mechanism for regulating IFN immune response. Using microarray and qRT-PCR assays, microRNA-221 (miR-221) was found to be significantly up-regulated in the serum samples from patients with HPV 16 infection, as well as in HPV 16-positive cervical cancer cells. miR-221 overexpression inhibited, while miR-221 knockdown facilitated HPV 16 E1-E2 mediated DNA replication in vitro. Moreover, overexpression of miR-221 was associated with upregulation of IFN-α and IFN-β at mRNA and protein levels in infected cells. Conversely, IFN-α and IFN-β mRNA or protein expression was significantly downregulated during inhibition of miR-221. Subsequently, we demonstrated that upregulation of miR-221 promoted the expression of representative interferon stimulated genes (ISGs) such as myxovirus protein A (MxA), 2',5'-oligoadenylate synthetases (OAS) and murine IFN-stimulated gene 15 (ISG15). In contrast, miR-221 inhibition significantly decreased ISGs expression. Furthermore, we found that suppressor of cytokine signaling 1 (SOCS1), a suppressor of interferon signaling pathway, was a direct target of miR-221 and overexpression of SOCS1 reversed the effects of miR-221 on the IFN-I response and HPV 16 E1-E2 mediated DNA replication. Collectively, the findings provide new evidence that miR-221 could inhibit HPV 16 E1-E2 mediated DNA replication through the SOCS1/Type I IFN signaling pathway suggesting it may be a novel anti-HPV therapeutic target.

Indexed as

DNA replicationHuman papillomavirus 16microRNA-221SOCS1/Type I IFN signaling pathway

Identifiers

PMID31933969
PMCPMC6947112
OpenAlexW3006457681

What OpenQuestion 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 OpenQuestion graph.