Evidence map›Paper›PMID 31322224›Full record

ArticleMolecular medicine reports2019

Inhibition of MCM2 enhances the sensitivity of ovarian cancer cell to carboplatin.

Minjie Deng, Jiajun Sun, Suhong Xie, Hui Zhen, Yanchun Wang, Ailing Zhong, Hongqin Zhang, Renquan Lu, Lin Guo

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

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  14. Multi-Omics Analysis of MCM2 as a Promising Biomarker in Pan-Cancer.Frontiers in cell and developmental biology · 2022
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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

9 authors at 1 institution in 1 country.

Minjie DengDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Jiajun SunDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Suhong XieDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Hui ZhenDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Yanchun WangDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Ailing ZhongDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Hongqin ZhangDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Renquan LuDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Lin GuoDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Fudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy is widely used for the treatment of ovarian cancer. Since chemotherapy resistance is the major cause of poor prognosis in patients with ovarian cancer, it is important to identify new methods to improve the efficacy of chemotherapy. Minichromosome maintenance complex component 2 (MCM2), which serves an essential role in DNA replication, has been recently identified as a novel proliferation marker with prognostic implications in multiple types of cancer. However, the role of MCM2 in ovarian cancer and its underlying molecular mechanisms remain unclear. Therefore, in the present study, the biological effects of MCM2 were investigated, particularly with respect to DNA damage and repair. In the present study, short hairpin RNA was employed to knockdown MCM2 expression in the A2780 ovarian cancer cell line. The sensitivity of A2780 cells to carboplatin was assessed by cell colony formation assay. The present results suggested that MCM2 knockdown inhibited the proliferation of tumor cells, induced G0/G1 phase arrest and did not exhibit effects on cell apoptosis. However, MCM2 knockdown significantly decreased the colony formation of A2780 cells treated with carboplatin. Furthermore, knockdown of MCM2 together with carboplatin treatment or UV irradiation increased the protein expression level of γ‑H2A histone family member X and p53 compared with control cells. The present data suggested that the increased sensitivity to carboplatin may occur via the p53‑dependent apoptotic response. Additionally, the present results suggested that knockdown of MCM2 may have therapeutic applications in enhancing the efficacy of carboplatin in patients with ovarian cancer.

Indexed as

RNA InterferenceAntineoplastic AgentsApoptosisCarboplatinCell Line, TumorDNA DamageFemaleHumansMinichromosome Maintenance Complex Component 2Ovarian NeoplasmsRNA, Small InterferingAntineoplastic AgentsCarboplatinMCM2 protein, humanMinichromosome Maintenance Complex Component 2RNA, Small Interfering

Identifiers

PMID31322224
PMCPMC6691261
OpenAlexW2959219552

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.