Evidence map›Paper›PMID 37081781›Full record

ArticleCancer medicine2023

Ginsenoside Rh2 attenuates the progression of non-small cell lung cancer by sponging miR-28-5p/STK4 axis and inactivating Wnt/β-catenin signaling.

Jun Ma, Di Zhao, Dahai Yu, Wei Song, Xiaofang Yang, Haitao Yin

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
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  5. The potential role of miR-155 in the tumorigenesis of cervical cancer.Frontiers in cell and developmental biology · 2025
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  7. Article
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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

6 authors at 2 institutions in 1 country.

Jun MaRadiotherapy Department, Affiliated Hospital of Nanjing University of Chinese Medicine, China.
Di ZhaoRadiotherapy Department, Affiliated Hospital of Nanjing University of Chinese Medicine, China.
Dahai YuRadiotherapy Department, Affiliated Hospital of Nanjing University of Chinese Medicine, China.
Wei SongRadiotherapy Department, Affiliated Hospital of Nanjing University of Chinese Medicine, China.
Xiaofang YangRadiotherapy Department, Affiliated Hospital of Nanjing University of Chinese Medicine, China.
Haitao YinRadiotherapy Department, Xuzhou Central Hospital, China.ORCID 0000-0002-4332-8773
Nanjing University of Chinese Medicine · CNXuzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGinsenoside Rh2 (G-Rh2) exerts anti-tumor activity in non-small cell lung cancer (NSCLC). microRNAs (miRNAs, miRs) play pivotal roles in NSCLC. We aimed to investigate whether G-Rh2 inhibited NSCLC progression by targeting miRNA.

methodsCell viability, apoptosis and cycle were determined by Cell Counting Kit-8, 6-diamidino-2-phenylindole (DAPI) staining and flow cytometry. The potential target miRNAs of G-Rh2 were screened by real-time quantitative polymerase chain reaction (RT-qPCR). The difference in miR-28-5p expression between lung adenocarcinoma (LUAD) tissues and normal tissues or lung squamous cell carcinoma (LUSC) tissues and normal tissues was retrieved from TCGA-LUAD and TCGA-LUSC, respectively. Kaplan-Meier Plotter was conducted to analyze the survival rate for different serine/threonine-protein kinase 4 (STK4) expressions with different prognostic risks. immunohistochemistry of STK4 expression in non-tumor and tumor tissues was analyzed from the HPA database. RT-qPCR and Western blot were adopted for detecting mRNA and protein expression. TargetScan V7.2, miRanda and PITA were adopted for predicting targets of miR-28-5p, overlapped genes were subjected to GO analysis. The interactions of miR-28-5p-Wnt and miR-28-5p-STK4 were detected by TOP/FOP luciferase reporter assay and dual luciferase reporter assay, respectively.

resultsCurrent study observed that G-Rh2 reduced miR-28-5p expression in NSCLC cells dose-dependently. miR-28-5p was upregulated in NSCLC tissues and cells. The target genes of miR-28-5p were enriched in negative regulation of Wnt signaling. miR-28-5p inhibitor inactivated Wnt signaling, inhibited cell viability and cell cycle, while enhanced cell apoptosis of NSCLC cells by targeting STK4. G-Rh2 exerted the similar effects with miR-28-5p inhibitor by reducing miR-28-5p. G-Rh2 and miR-28-5p inhibitor exerted a synergistic effect on inhibiting NSCLC tumor growth.

conclusionIn conclusion, G-Rh2 attenuates NSCLC development by affecting miR-28-5p/STK4 axis and inactivating Wnt signaling. Taken together, we project out a novel therapeutic target for NSCLC.

Indexed as

Adenocarcinoma of LungCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellLung NeoplasmsMicroRNAsbeta CateninCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGinsenosidesHippo KinasesHumansIntracellular Signaling Peptides and ProteinsLuciferasesProtein Serine-Threonine KinasesWnt Signaling Pathwaybeta Cateninginsenoside Rh2GinsenosidesHippo KinasesIntracellular Signaling Peptides and ProteinsLuciferasesMicroRNAsMIRN28 microRNA, humanProtein Serine-Threonine KinasesSTK4 protein, humanginsenoside Rh2 (G-Rh2)miR-28-5p/STK4 axisnon-small cell lung cancer (NSCLC)tumor growthWnt/β-catenin signaling

Identifiers

PMID37081781
PMCPMC10278491
OpenAlexW4366603319

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.