Evidence map›Paper›PMID 39557898›Full record

ArticleScientific reports2024

Down-regulation of ESRP2 inhibits breast cancer cell proliferation via inhibiting cyclinD1.

Caiping He, Yuting Chen, Ximin Zhang, Huancun Feng, Yuzhen Rao, Tangyang Ji, Wenya Wang

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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

7 authors.

Caiping He *School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Yuting Chen *School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Ximin ZhangSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Huancun FengSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Yuzhen RaoSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Tangyang JiSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Wenya WangSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China. wangwy@smu.edu.cn.

Funding

Natural Science Foundation of Guangdong Provice No2023A1515010454Natural Science Foundation of Guangdong Province No2022A1515010877Science Communication Professional Committee of Chinese Pharmaceutical Association NoCMEI2024KPYJ00113
6 · The paper itself

Abstract

Epithelial splicing regulatory protein 2 (ESRP2),an important alternative splicing protein of mRNA, is reported to have a dual role in tumors, which can promote or inhibit the occurrence and development of tumors. However, the function and mechanism of ESRP2 in breast cancer (BC) remain unclear. The distribution of ESRP2 expression in breast cancer and the correlation between ESRP2 expression and the overall survival rate were detected by The Cancer Genome Atlas (TCGA) database. Gene Ontology(GO)analysis, containing biological process, cellular components, and molecular function, was utilized to evaluate the potential mechanism of ESRP2 in breast cancer. The ESRP2 expression in breast cancer cell lines was detected by real-time quantitative PCR analysis (RT-qPCR) and western blotting. Cell clone was performed to examine the proliferation of ESRP2 knockdown in MCF-7 cells. The cell cycle was measured by flow cytometry assays. The role of ESRP2 knockdown in synergistic effect with chemotherapeutic agents was also determined by MTT assay. Bioinformatics analysis demonstrated that the ESRP2 gene was elevated in breast cancer cells and its overexpression was strongly correlated with shorter overall survival. GO analysis revealed that ESRP2 expression was related to cell proliferation. ESRP2 mRNA and protein expression were elevated in breast cancer cell lines, compared to the normal human breast cell line MCF-10 A. Dwon-regulation of ESRP2 inhibited cell proliferation and promoted the sensitivity of chemotherapy drug, Cisplatin(DDP) and Paclitaxel (TAXOL), in MCF-7 cells.Additionally, ESRP2 knockdown obstructed the cell cycle at the G1 phase and caused a decrease in cyclinD1 protein expression. These findings reveal that ESRP2 is highly expressed in breast cancer and is correlated with poor prognosis in breast cancer patients. ESRP2 knockdown can inhibit MCF-7 cell proliferation by arresting the cell cycle at the G1 phase and promoting the sensitivity of chemotherapy drugs (DDP and TAXOL)in MCF-7 cells. ESRP2 may be required for the regulation of breast cancer progression, as well as a critical target for the clinical treatment of breast cancer.

Indexed as

Breast NeoplasmsCell ProliferationCyclin D1Gene Expression Regulation, NeoplasticAntineoplastic AgentsCell Line, TumorCisplatinDown-RegulationFemaleHumansMCF-7 CellsPaclitaxelRNA-Binding ProteinsAntineoplastic AgentsCCND1 protein, humanCisplatinCyclin D1PaclitaxelRNA-Binding ProteinsBreast cancerCell proliferationESRP2Potential biomarker

Identifiers

PMID39557898
PMCPMC11574003

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.