Evidence map›Paper›PMID 33893080›Full record

ArticleCancer genomics & proteomics

Effect of HPV 16 E6 Oncoprotein Variants on the Alterations of the Proteome of C33A Cells.

Olga Lilia Garibay-Cerdenares, Luz Victoria Sánchez-Meza, Sergio Encarnación-Guevara, Magdalena Hernández-Ortíz, Gabriel Martínez-Batallar, Francisco Israel Torres-Rojas, Miguel Ángel Mendoza-Catalán, Oscar Del Moral-Hernández, Marco Antonio Leyva-Vázquez, Berenice Illades-Aguiar

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Chaperonin in health and disease.Molecular biomedicine · 2026
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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 1 institution in 1 country.

Olga Lilia Garibay-CerdenaresLaboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, México.
Luz Victoria Sánchez-MezaLaboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, México.
Sergio Encarnación-GuevaraLaboratorio de Proteómica, Centro de Ciencias Genómicas-UNAM, Cuernavaca, México.
Magdalena Hernández-OrtízLaboratorio de Proteómica, Centro de Ciencias Genómicas-UNAM, Cuernavaca, México.
Gabriel Martínez-BatallarLaboratorio de Proteómica, Centro de Ciencias Genómicas-UNAM, Cuernavaca, México.
Francisco Israel Torres-RojasLaboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, México.
Miguel Ángel Mendoza-CatalánLaboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, México.
Oscar Del Moral-HernándezLaboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, México.
Marco Antonio Leyva-VázquezLaboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, México.
Berenice Illades-AguiarLaboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, México; billades@uagro.mx.
Universidad Autónoma de Guerrero · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimThe E6 genotypic variants of HPV 16 identified in lesions of women with cervical cancer (CC) in Southern of Mexico include the E-G350, AAa, AAc, E-C188/G350, and E-A176/G350, transcriptomic analysis cells transfected with those variants showed to induce differential expression of the host genes involved in the development of CC, the aim of this work was to understand how the over-expression of the E6 oncoprotein and its variants can induce molecular mechanisms that lead to more aggressive HPV 16 phenotypes in cervical cancer and which proteins could be associated with the process. MATERIALS AND

methodsTotal extracts from C33A, C33A mock, C33A AAa, C33A E-C188/G350, C33A E-A176/G350, and C33A E-prototype cells were analyzed using 2D electrophoresis, PDQuest software and mass spectrometry, validation of results was performed through qPCR.

resultsStatistically significant differential expression of 122 spots was detected, 12 of the identified proteins were associated with metabolism and metabolic programming. Out of these CCT8, ENO and ALDH1A were further validated.

conclusionCCT8 and ALDH1A were found to be over-expressed in C33A AAa and C33A E-A176/G350, compared to the E prototype. Both proteins could be associated with a most aggressive phenotype due to their relationship with metabolism, protein folding and stemness, mechanisms associated to E6 that could be useful in the design of new therapies.

Indexed as

Human papillomavirus 16Oncogene ProteinsOncogene Proteins, ViralProteomicsRepressor ProteinsUterine Cervical NeoplasmsFemaleHumansProteomeE6 protein, Human papillomavirus type 16Oncogene ProteinsOncogene Proteins, ViralProteomeRepressor Proteins2D electrophoresiscervical cancerHPV 16 E6 variantsproteomic analysis

Identifiers

PMID33893080
PMCPMC8126335
OpenAlexW3154217440

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.