Evidence map›Paper›PMID 41993883›Full record

ArticleComputational and structural biotechnology journal2026

Systems Analysis of miRNA-Mediated Host Regulatory Response in HPV-Associated Cervical Malignancy.

Ishrat Khan, N S Suneesh, R Harshithkumar, Ashwini More, Shyam Sundar Nandi, Abdul Arif Khan, Anupam Mukherjee

Abstract read
In one paragraph

Article in Computational and structural biotechnology journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Ishrat KhanICMR-National Institute of Virology, Pune 400001, Maharashtra, India.ORCID https://orcid.org/0009-0007-1610-0937
N S SuneeshICMR-National Institute of Virology, Pune 400001, Maharashtra, India.
R HarshithkumarICMR-National Institute of Translational Virology and AIDS Research, Pune 400026, Maharashtra, India.ORCID https://orcid.org/0000-0002-7569-4815
Ashwini MoreICMR-National Institute of Translational Virology and AIDS Research, Pune 400026, Maharashtra, India.
Shyam Sundar NandiICMR-National Institute of Virology, Pune 400001, Maharashtra, India.
Abdul Arif KhanDepartment of Biotechnology, Savitribai Phule Pune University, Pune 411007, MH, India.
Anupam MukherjeeICMR-National Institute of Virology, Pune 400001, Maharashtra, India.ORCID https://orcid.org/0000-0002-0612-2258

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent high-risk human papillomavirus (HPV) infection, particularly types 16 and 18, is the primary driver of cervical carcinogenesis. These viruses utilize viral oncoproteins to manipulate host gene expression through multiple regulatory mechanisms. Within this landscape, microRNAs (miRNAs) emerge as critical posttranscriptional modulators that contribute to the dysregulation of pathways involved in cellular transformation and tumor progression. In this study, we investigated HPV-associated miRNA dysregulation using HPV-negative (C33A) and HPV-positive (SiHa, HeLa) cervical cancer cell lines, integrating custom microarray profiling with comprehensive systems biology and bioinformatic analyses. Our results identified 42 dysregulated miRNAs, including hsa-miR-125b-5p, hsa-miR-106b-5p, hsa-miR-23b-3p, and hsa-miR-30d-5p, which were significantly down-regulated across all experimental models. Integration of these miRNAs with cervical carcinoma transcriptomic data (GSE151666) revealed that HPV16 and HPV18 distinctly remodel host gene networks to drive malignancy. Network analysis pinpointed specific regulatory hubs, such as

Identifiers

PMID41993883
PMCPMC13082576

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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 OpenQuestion graph.