ArticleInternational journal of gynecological cancer : official journal of the International Gynecological Cancer Society2014
S-phase cell cycle arrest, apoptosis, and molecular mechanisms of aplasia ras homolog member I-induced human ovarian cancer SKOV3 cell lines.
Article in International journal of gynecological cancer : official journal of the International Gynecological Cancer Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 22 citations in OpenAlex.
- Integrated In Silico and In Vitro Study of Copper Nanocatalyzed Carbonyl-Functionalized Triazoles-Inducing S Phase Cell Cycle Arrest and Apoptosis in MCF-7.ChemistryOpen · 2026Article
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- TIPE2 Induced the Proliferation, Survival, and Migration of Lung Cancer Cells Through Modulation of Akt/mTOR/NF-κB Signaling Cascade.Biomolecules · 2019Article
- Normobaric hyperoxia inhibits the progression of lung cancer by inducing apoptosis.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- A Novel Selective JAK2 Inhibitor Identified Using Pharmacological Interactions.Frontiers in pharmacology · 2018Article
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectiveAplasia Ras homolog member I (ARHI) is associated with human ovarian cancer (HOC) growth and proliferation; however, the mechanisms are unclear. The purpose of this study was to investigate ARHI effects in HOC SKOV3 cells.
methodsWe transfected SKOV3 cells with PIRES2-EGFP-ARHI and measured growth inhibition rates, cell cycle distribution, apoptosis rates, and expression of P-STAT3 (phosphorylated signal transduction and activators of transcription 3) and P-ERK (phosphorylated extracellular signal regulated protein kinase).
resultsOur data showed significant inhibition of growth, significantly increased S-phase arrest and apoptosis rates, and reduction of P-STAT3 and P-ERK1/2 expression levels.
conclusionsWe propose the mechanism may involve ARHI-induced phosphorylation of ERK1/2 and STAT3 protein kinases, thereby blocking proliferation signaling pathways, to induce HOC SKOV3 apoptosis.
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