Evidence map›Paper›PMID 38028209›Full record

ArticleSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2023

Transcriptomics analyses reveal the effects of Pentagamaboronon-0-ol on PI3K/Akt and cell cycle of HER2+ breast cancer cells.

Adam Hermawan, Febri Wulandari, Rohmad Yudi Utomo, Ratna Asmah Susidarti, Mitsunori Kirihata, Edy Meiyanto

Open access · hybridAbstract read
In one paragraph

Article in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 22% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

6 authors at 2 institutions in 1 country.

Adam HermawanLaboratory of Macromolecular Engineering, Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, 55281, Yogyakarta, Indonesia.
Febri WulandariCancer Chemoprevention Research Center, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, 55281, Yogyakarta, Indonesia.
Rohmad Yudi UtomoCancer Chemoprevention Research Center, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, 55281, Yogyakarta, Indonesia.
Ratna Asmah SusidartiCancer Chemoprevention Research Center, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, 55281, Yogyakarta, Indonesia.
Mitsunori KirihataResearch Center for BNCT, Osaka Metropolitan University, 1-2, Gakuen-cho, Naka-ku, Sakai, Osaka 599-8570, Japan.
Edy MeiyantoLaboratory of Macromolecular Engineering, Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, 55281, Yogyakarta, Indonesia.
Universitas Gadjah Mada · IDOsaka Metropolitan University

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Monoclonal antibodies and targeted therapies against HER2+ breast cancer has improved overall and disease-free survival in patients; however, encountering drug resistance causes recurrence, necessitating the development of newer HER2-targeted medications. A curcumin analog PGB-0-ol showed most cytotoxicity against HCC1954 HER2+ breast cancer cells than against other subtypes of breast cancer cells. Objective: Here, we employed next-generation sequencing technology to elucidate the molecular mechanism underlying the effect of PGB-0-ol on HCC1954 HER2+ breast cancer cells. Methods: The molecular mechanism underlying the action of PGB-0-ol on HCC1954 HER2+ breast cancer cells was determined using next-generation sequencing technologies. Additional bioinformatics studies were performed, including gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, disease-gene, and drug-gene associations, network topology analysis (NTA), and gene set enrichment analysis (GSEA). Results: We detected 2,263 differentially expressed genes (DEGs) (1,459 upregulated and 804 downregulated) in the PGB-0-ol- and DMSO-treated HCC1954 cells. KEGG enrichment data revealed the control of phosphatidylinositol signaling system, and ErbB signaling following PGB-0-ol treatment. Gene ontology (GO) enrichment analysis demonstrated that these DEGs governed cell cycle, participated in the mitotic spindle and nuclear membrane, and controlled kinase activity at the molecular level. According to the NTA data for GO enrichment, GSEA data for KEGG, drug-gene and disease-gene, PGB-0-ol regulated PI3K/Akt signaling and cell cycle in breast cancer. Overall, our investigation revealed the transcriptomic profile of PGB-0-ol-treated HCC1954 breast cancer cells following PGB-0-ol therapy. Bioinformatics analyses showed that PI3K/Akt signaling and cell cycle was modulated. However, further studies are required to validate the findings of this study.

Indexed as

AnticancerDrug developmentHER2+ breast cancerPGB-0-olTranscriptomics

Identifiers

PMID38028209
PMCPMC10652209
OpenAlexW4387953128

What OpenQuestion holds

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LicenceCC BY
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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.