Evidence map›Paper›PMID 37812599›Full record

ArticlePloS one2023

The HPV-TP53-MALAT1 Axis: Unravelling interactions in cervical cancer development.

Saba Iordanishvili, Tornike Metreveli, Elene Lipartia, Konstantine Gachechiladze, Irakli Khuntsaria, Tamar Qobulashvili, Mariam Jorbenadze, Tamaz Revazishvili, Ekaterina Kldiashvili, Andreas Martin Kaufmann

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Long noncoding HOXD-AS1: a crucial regulator of malignancy.Frontiers in cell and developmental biology · 2025
    Review
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

10 authors at 2 institutions in 2 countries.

Saba IordanishviliPetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.
Tornike MetreveliPetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.
Elene LipartiaPetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.
Konstantine GachechiladzePetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.
Irakli KhuntsariaPetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.
Tamar QobulashviliPetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.
Mariam JorbenadzePetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.
Tamaz RevazishviliPetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.
Ekaterina KldiashviliPetre Shotadze Tbilisi Medical Academy, Tbilisi, Georgia.ORCID 0000-0003-1764-7778
Andreas Martin KaufmannCharite Universitatsmedizin Berlin, Berlin, Germany.
Petre Shotadze Tbilisi Medical Academy · GECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCervical cancer, primarily driven by Human Papillomavirus (HPV) infection, stands as a substantial global health challenge. The TP53 gene's, Arg72Pro polymorphism has emerged as a noteworthy player in cervical cancer development, particularly among individuals harboring high-risk (HR) HPV types. Additionally, long non-coding RNAs (lncRNAs), exemplified by metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), exert critical roles in cancer biology. This study delves into unravelling the intricate connections linking HPV infection, TP53 Arg72Pro polymorphism, and MALAT1 expression in the context of cervical cancer. MATERIALS AND

methodsWithin a cohort of cervical cancer patients, we discerned HPV infection statuses, executed genotyping for the TP53 Arg72Pro polymorphism, and quantified MALAT1 expression through quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Statistical analyses meticulously probed relationships intertwining HPV infection, TP53 polymorphism, and MALAT1 expression.

findingsOur investigation revealed a striking prevalence of the TP53 Arg72Pro polymorphism among HPV-positive subjects, accompanied by a robust and statistically significant correlation linking MALAT1 overexpression (p<0.01) and HR-HPV positivity (p<0.03). Importantly, a subset of MALAT1 overexpression cases unveiled a concomitant TP53 Pro72Pro polymorphism. In contrast, HPV-negative invasive cervical carcinoma samples exhibited no discernible shifts in MALAT1 expression.

conclusionThe contours of our findings sketch a compelling landscape wherein HR-HPV infection, TP53 polymorphism, and MALAT1 expression intertwine significantly in cervical cancer. The voyage ahead entails delving deeper into molecular underpinnings to decipher MALAT1's nuanced role and its dance with TP53 within HPV-associated cervical carcinogenesis. This expedition promises insights that may engender targeted therapeutic interventions and bespoke prognostic markers, tailored to the realm of HR-HPV-related cervical cancer.

Indexed as

AdenocarcinomaPapillomavirus InfectionsRNA, Long NoncodingTumor Suppressor Protein p53Uterine Cervical NeoplasmsFemaleHumansPolymorphism, GeneticMALAT1 long non-coding RNA, humanRNA, Long NoncodingTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID37812599
PMCPMC10561830
OpenAlexW4387450415

What Socratic holds

Textmetadata
LicenceCC BY
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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.