Evidence map›Paper›PMID 36164345›Full record

ArticleJournal of oncology2022

miR-187/PDLIM1 Gets Involved in Gastric Cancer Progression and Cisplatin Sensitivity of Cisplatin by Mediating the Hippo-YAP Signaling Pathway.

Yeru Tan, Yuehua Li, Hongbo Zhu, Xiaoping Wu, Kai Mei, Pian Li, Qiao Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

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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

7 citing papers in PubMed.

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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

7 authors.

Yeru TanThe First Affiliated Hospital, Department of Medical Oncology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.ORCID https://orcid.org/0000-0003-2720-4348
Yuehua LiThe First Affiliated Hospital, Department of Medical Oncology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Hongbo ZhuThe First Affiliated Hospital, Department of Medical Oncology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.ORCID https://orcid.org/0000-0002-2462-2192
Xiaoping WuThe First Affiliated Hospital, Department of Medical Oncology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Kai MeiThe First Affiliated Hospital, Department of Oncology Radiotherapy, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Pian LiThe First Affiliated Hospital, Department of Oncology Radiotherapy, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Qiao YangThe First Affiliated Hospital, Department of Oncology Radiotherapy, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.ORCID https://orcid.org/0000-0001-8739-6674

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is one of the most prevalent malignancies in the digestive system across the world. The function and mechanism of PDLIM1, a cancer-suppressing gene, in gastric cancer progression remain unclear. This study is aimed at investigating the expression features and function of PDLIM1 in GC. RT-qPCR and western blot were used to compare the profiles of PDLIM1 and miR-187 between GC and normal tissues. The cell models of PDLIM1 overexpression and low expression were established in gastric cancer cell lines MKN45 and AGS. CCK8 and BrdU assays measured cell proliferation. Flow cytometry monitored cell apoptosis. Transwell analyzed cell invasion and migration. The influence of miR-187 overexpression on gastric cancer development was assessed. We predicted the targeted correlation between miR-187 and PDLIM1 through bioinformatics, which was corroborated via dual luciferase activity assay and RIP. Meanwhile, the cell model of PDLIM1 overexpression was built in AGS cells transfected with miR-187 mimics. A rescue experiment was conducted to assess the impact of PDLIM1 overexpression on the procancer function of miR-187. As a result, in contrast with normal paracancer tissues, PDLIM1 was substantially downregulated in GC tissues. Moreover, PDLIM1 overexpression considerably dampened proliferation, invasion, and migration in GC cells, boosted the cell apoptosis, and bolstered their sensitivity to cisplatin. PDLIM1 knockdown or miR-187 overexpression dramatically fostered GC cell proliferation, invasion, and migration and repressed cell apoptosis. Mechanism studies demonstrated that PDLIM1 vigorously restrained the profiles of the Hippo-YAP signaling pathway and the downstream target genes. miR-187 targeted PDLIM1, while miR-187 overexpression cramped PDLIM1 expression. The rescue experiment suggested that PDLIM1 overexpression weakened the procancer function of miR-187 in GC cells. In conclusion, our study demonstrated that PDLIM1 presented a low expression in GC tissues, while miR-187/PDLIM1 participated in GC development and cisplatin sensitivity by mediating the Hippo-YAP signaling pathway.

Identifiers

PMID36164345
PMCPMC9509220

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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.