ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2012
Effects of ARHI on cell cycle progression and apoptosis levels of breast cancer cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Transcriptional silencing of long noncoding RNA GNG12-AS1 uncouples its transcriptional and product-related functions.Nature communications · 2016Article
- Characterization of age signatures of DNA methylation in normal and cancer tissues from multiple studies.BMC genomics · 2014Article
- ARHI (DIRAS3) induces autophagy in ovarian cancer cells by downregulating the epidermal growth factor receptor, inhibiting PI3K and Ras/MAP signaling and activating the FOXo3a-mediated induction of Rab7.Cell death and differentiation · 2014Article
- Over-expression of ARHI decreases tumor growth, migration, and invasion in human glioma.Medical oncology (Northwood, London, England) · 2014Article
- Effects of ARHI on breast cancer cell biological behavior regulated by microRNA-221.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Imprinted chromatin around DIRAS3 regulates alternative splicing of GNG12-AS1, a long noncoding RNA.American journal of human genetics · 2013Article
- Effect of ARHI on lung cancer cell proliferation, apoptosis and invasion in vitro.Molecular biology reports · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purposes of this study were to investigate the role of Aplysia Ras Homolog I (ARHI) on cell growth, proliferation, apoptosis, and other biological characteristics of HER2-positive breast cancer cells. Our goal was to provide experimental evidence for the development of future effective treatments of HER2-positive breast cancer. A pcDNA3.1-ARHI eukaryotic expression vector was constructed and transfected into the human HER2-positive breast cancer cell lines SK-BR-3 and JIMT-1. Then, various experimental methods were utilized to analyze the biological characteristics of ARHI-expressing breast cancer cells and to examine the impact of expression of the ARHI gene on cyclin D1, p27(Kip1), and calpain1 expression. We further analyzed the cells in each group after treatment with trastuzumab to examine the effects of this drug on various cellular characteristics. When we compared pcDNA3.1-ARHI-expressing SK-BR-3 and JIMT-1 cells to their respective empty vector and control groups, we found that cell viability was significantly lower (p < 0.05) in the ARHI-expressing cells, and the proportions of G1 phase cells and apoptotic cells were significantly higher in the ARHI-expressing cells (p < 0.05). In all groups of SK-BR-3 cells, trastuzumab treatment significantly decreased cell growth (p < 0.05). The proportion of cells in G1 phase and the number of apoptotic cells in the pcDNA3.1-ARHI-expressing group were significantly higher than that in the empty vector group and the control group (p < 0.05). The growth of pcDNA3.1-ARHI-transfected JIMT-1 cells was significantly decreased (p < 0.05), while the proportion of apoptotic cells was significantly increased (p < 0.05). Cell growth, viability, and the percentage of apoptotic cells were similar between the JIMT-1 empty vector and control groups. ARHI expression inhibited cyclin D1 expression in SK-BR-3 cells and JIMT-1 cells, while it promoted p27(Kip1) and calpain1 expression in these cells. ARHI expression inhibits the growth and proliferation of HER2-positive breast cancer cells, while it also promotes apoptosis in these cells. ARHI expression also improves the sensitivity of JIMT-1 cells to trastuzumab by inducing apoptosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.