ArticleDigestive diseases and sciences2012
Knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells.
Article in Digestive diseases and sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Diverse roles of FOXO family members in gastric cancer.World journal of gastrointestinal oncology · 2021Review
- The role of AP-1 in self-sufficient proliferation and migration of cancer cells and its potential impact on an autocrine/paracrine loop.Oncotarget · 2018Article
- FOXO1: Another avenue for treating digestive malignancy?Seminars in cancer biology · 2018Review
- RON is overexpressed in bladder cancer and contributes to tumorigenic phenotypes in 5637 cells.Oncology letters · 2018Article
- Monoclonal antibody Zt/g4 targeting RON receptor tyrosine kinase enhances chemosensitivity of bladder cancer cells to Epirubicin by promoting G1/S arrest and apoptosis.Oncology reports · 2017Article
- Strategies of targeting the extracellular domain of RON tyrosine kinase receptor for cancer therapy and drug delivery.Journal of cancer research and clinical oncology · 2016Review
- The RON receptor tyrosine kinase is a potential therapeutic target in Burkitt lymphoma.Cancer biology & therapy · 2013Article
- Therapeutic targets for cancer: current concepts with PI 3-K, Akt, & mTOR.The Indian journal of medical research · 2013Article
- Targeting disease through novel pathways of apoptosis and autophagy.Expert opinion on therapeutic targets · 2012Review
- A Critical Kinase Cascade in Neurological Disorders: PI 3-K, Akt, and mTOR.Future neurology · 2012Article
- Shedding new light on neurodegenerative diseases through the mammalian target of rapamycin.Progress in neurobiology · 2012Review
- PRAS40 is an integral regulatory component of erythropoietin mTOR signaling and cytoprotection.PloS one · 2012Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsAltered Recepteur d'Origine nantais (RON) expression transduces signals inducting invasive growth phenotype that includes cell proliferation, migration, matrix invasion, and protection of apoptosis in human cancer cells. The aims of the current study were to evaluate whether RON affects tumor cell behavior and cellular signaling pathways including activator protein-1 (AP-1) and Akt/forkhead box O (FoxO) in human colorectal cancer cells.
methodsTo study the biological role of RON on tumor cell behavior and cellular signaling pathways in human colorectal cancer, we used small interfering RNA (siRNA) to knockdown RON gene expression in human colorectal cancer cell line, DKO-1.
resultsKnockdown of RON diminished migration, invasion, and proliferation of human colorectal cancer cells. Knockdown of RON decreased AP-1 transcriptional activity and expression of AP-1 target genes. Knockdown of RON activated cleaved caspase-3, -7, -9, and PARP, and down-regulated the expression of Mcl-1, survivin and XIAP, leading to induction of apoptosis. Knockdown of RON induced cell cycle arrest in the G2/M phase of cancer cells by an increase of p27 and a decrease of cyclin D3. Knockdown of RON inhibited the phosphorylation of Akt/FoxO signaling proteins such as Ser473 and Thr308 of Akt and FoxO1/3a.
conclusionsThese results indicate that knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells.
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