Evidence map›Paper›PMID 38838436›Full record

ReviewTranslational oncology2024

RBM15 facilities lung adenocarcinoma cell progression by regulating RASSF8 stability through N6 Methyladenosine modification.

Mingsheng Ma, Wei Wang, Li Li, Xiaoyan Wang, Qiubo Huang, Chen Zhou, Yunchao Huang, Guangqiang Zhao, Lianhua Ye

Abstract readReview
In one paragraph

Review in Translational oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
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  10. Review
  11. Article
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  13. RBM15-mediated mFrontiers in cell and developmental biology · 2025
    Review
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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.

Mingsheng MaDepartment of Thoracic Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan,650118, China; Department of Thoracic Surgery, The Sixth Affiliated Hospital of Kunming Medical University, Yuxi, Yunnan,653100, China.
Wei WangDepartment of Thoracic Surgery, Taihe Hospital (Hubei University of Medicine), Shiyan, Hubei,442000, China.
Li LiDepartment of Biotherapy Chemotherapy Center, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan,650118, China.
Xiaoyan WangDepartment of Thoracic Surgery, The Sixth Affiliated Hospital of Kunming Medical University, Yuxi, Yunnan,653100, China.
Qiubo HuangDepartment of Thoracic Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan,650118, China.
Chen ZhouDepartment of Thoracic Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan,650118, China.
Yunchao HuangDepartment of Thoracic Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan,650118, China.
Guangqiang ZhaoDepartment of Thoracic Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan,650118, China.
Lianhua YeDepartment of Thoracic Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan,650118, China. Electronic address: lhye1204@aliyun.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invasion and migration are the primary factors for mortality in lung adenocarcinoma (LUAD) patients. The precise role of RNA-binding motif protein15 (RBM15)-mediated m6A modification in LUAD is not yet fully clarified. This research aims to elucidate the mechanism of RBM15 in the invasion and migration of LUAD. Western blot and dot blot assay results showed that RBM15 and methylation levels of m6A were highly expressed in LUAD tissues. Overexpression of RBM15 by lentivirus transfection increased m6A levels and promoted the invasion, migration, and proliferation of A549 and H1734 cells. Knockdown of RBM15 by lentivirus transfection had opposite effects on m6A levels, invasion, migration, and proliferation of A549 and H1734 cells. The results of nude mouse proliferation models confirmed that RBM15 knockdown inhibited in vivo tumor proliferation . Sequencing and immunoprecipitation identified RASSF8 as an interacting protein of RBM15 involved in cell invasion and migration. RBM15-mediated m6A modification inhibited RASSF8 protein levels and increased LUAD cell invasion and migration. The rescue assays demonstrated that the regulation of RBM15 on LUAD cell invasion and migration was partially rescued by RASSF8. In conclusion, RBM15-mediated m6A modification inhibits the RASSF8 protein levels and increases cell invasion and migration. Thus, targeting the RBM15-m6A-RASSF8 axis may be a promising strategy for repressing LUAD cell invasion and migration.

Indexed as

Lung adenocarcinomaN6-methyladenosine (m6A)RASSF8RNA binding motif protein 15 (RBM15)

Identifiers

PMID38838436
PMCPMC11214523

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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.