Evidence map›Paper›PMID 37294480›Full record

ArticleMedical oncology (Northwood, London, England)2023

The crosstalk between ubiquitin-conjugating enzyme E2Q1 and p53 in colorectal cancer: An in vitro analysis.

Maryam Rasouli, Sara Khakshournia, Omid Vakili, Sanaz Dastghaib, Atefeh Seghatoleslam, Sayed Mohammad Shafiee

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. 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

6 authors at 2 institutions in 1 country.

Maryam Rasouli *Department of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID http://orcid.org/0000-0001-5137-7068
Sara Khakshournia *Department of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID http://orcid.org/0000-0003-4207-0114
Omid VakiliAutophagy Research Center, Department of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Zand Street, Shiraz, 71348-14336, Iran.ORCID http://orcid.org/0000-0002-9103-872X
Sanaz DastghaibEndocrinology and Metabolism Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID http://orcid.org/0000-0001-8553-9221
Atefeh SeghatoleslamDepartment of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID http://orcid.org/0000-0002-8277-6608
Sayed Mohammad ShafieeAutophagy Research Center, Department of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Zand Street, Shiraz, 71348-14336, Iran. shafieem@sums.ac.ir.ORCID http://orcid.org/0000-0002-9221-2267
Shiraz University of Medical Sciences · IRIsfahan University of Medical Sciences · IR

Funding

Vice-Chancellor for Research, Shiraz University of Medical Sciences 93-05-29-7123
6 · The paper itself

Abstract

Colorectal cancer (CRC) is a prevalent gastrointestinal neoplasm that ranks fourth in terms of cancer-related deaths worldwide. In the process of CRC progression, multiple ubiquitin-conjugating enzymes (E2s) are involved; UBE2Q1 is one of those newly identified E2s that is markedly expressed in human colorectal tumors. Since p53 is a well-known tumor suppressor and defined as a key factor to be targeted by the ubiquitin-proteasome system, we hypothesized that UBE2Q1 might contribute to CRC progression through the modulation of p53. Using the lipofection method, the cultured SW480 and LS180 cells were transfected with the UBE2Q1 ORF-containing pCMV6-AN-GFP vector. Then, quantitative RT-PCR was used to assay the mRNA expression levels of p53's target genes, i.e., Mdm2, Bcl2, and Cyclin E. Moreover, Western blot analysis was performed to confirm the cellular overexpression of UBE2Q1 and assess the protein levels of p53, pre- and post-transfection. The expression of p53's target genes were cell line-dependent except for Mdm2 that was consistent with the findings of p53. The results of Western blotting demonstrated that the protein levels of p53 were greatly lower in UBE2Q1-transfected SW480 cells compared to the control SW480 cells. However, the reduced levels of p53 protein were not remarkable in the transfected LS180 cells compared to the control cells. The suppression of p53 is believed to be the result of UBE2Q1-dependent ubiquitination and its subsequent proteasomal degradation. Furthermore, the ubiquitination of p53 can act as a signal for degradation-independent functions, such as nuclear export and suppressing the p53's transcriptional activities. In this context, the decreased Mdm2 levels can moderate the proteasome-independent mono-ubiquitination of p53. The ubiquitinated p53 modulates the transcriptional levels of target genes. Therefore, the up-modulation of UBE2Q1 may influence the transcriptional activities depending on p53, and thereby contributes to CRC progression through regulating the p53.

Indexed as

Colorectal NeoplasmsUbiquitin-Conjugating EnzymesHumansProteasome Endopeptidase ComplexProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53UbiquitinationProteasome Endopeptidase ComplexProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53UBE2Q1 protein, humanUbiquitin-Conjugating EnzymesBcl2Colorectal neoplasmsCyclin EMdm2Tumor suppressor protein p53UBE2Q1

Identifiers

PMID37294480
OpenAlexW4379966990

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.