Evidence map›Paper›PMID 33976698›Full record

ArticleJournal of oncology2021

Nucleolin Promotes Cisplatin Resistance in Cervical Cancer by the YB1-MDR1 Pathway.

Jing Ke, Chunming Gu, Heyan Zhang, Yang Liu, Wenhao Zhang, Huiling Rao, Shan Li, Fuyun Wu

Open access · hybridAbstract read
In one paragraph

Article in Journal of oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 3 syntheses or guidelines pooled it, 20 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Jing KeSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.ORCID https://orcid.org/0000-0002-9181-6042
Chunming GuSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.ORCID https://orcid.org/0000-0002-9967-5723
Heyan ZhangSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.ORCID https://orcid.org/0000-0002-2466-9636
Yang LiuSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.ORCID https://orcid.org/0000-0002-2142-7738
Wenhao ZhangSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.ORCID https://orcid.org/0000-0001-6352-6470
Huiling RaoSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.ORCID https://orcid.org/0000-0003-3332-1479
Shan LiSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.ORCID https://orcid.org/0000-0003-2577-0653
Fuyun WuSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.ORCID https://orcid.org/0000-0002-2078-379X
Hubei University of Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeCervical cancer is the fourth most common cancer in women worldwide and is the main cause of cancer-related deaths in women. Cisplatin (DDP) is one of the major chemotherapeutic drugs for cervical cancer patients. But, drug resistance limits the effectiveness of cancer therapy. Nucleolin (NCL) is a nucleocytoplasmic multifunctional protein involved in the development of cancer. It has been reported that NCL may be a potential target for modulation of drug resistance. However, the precise molecular mechanisms are poorly understood. MATERIALS AND

methodsHuman cervical cancer Hela cells and their cisplatin-resistant cell line Hela/DDP were used in this study. The protein level of NCL in cervical cancer cells was measured by western blot analysis. Hela cells and Hela/DDP cells were transfected with NCL overexpression plasmid or NCL siRNA separately. MTT and EdU assay were performed to evaluate the cell viability and sensitivity to cisplatin. The drug efflux function of MDR1 protein was assessed by intracellular rhodamine-123 accumulation assay.The promoter activity of MDR1 was assessed by using a dual-luciferase reporter assay.

resultsWe found that the protein level of NCL was elevated in Hela/DDP cells. Overexpression of NCL increased cervical cancer cell proliferation and attenuated the sensitivity to cisplatin. Overexpression of NCL increased Multidrug resistance (MDR1) gene expression and drug efflux. Our results demonstrated that NCL was highly related with cisplatin resistance in cervical cancer. NCL played an important role in MDR1 gene transcription through regulation of the transcription factor YB1.

conclusionOur findings revealed the novel role of NCL in cisplatin-resistant cervical cancer and NCL may be a potential therapeutic target for chemoresistance.

Identifiers

PMID33976698
PMCPMC8084676
OpenAlexW3158603138

What OpenQuestion holds

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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.