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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Antineoplastic Agents, Arsenic Trioxide, Arsenicals, Base Sequence, Blotting, Western, Bone Morphogenetic Proteins, Carcinoma, Cell Line, Tumor, Colorectal Neoplasms, Esophageal Neoplasms, Gene Expression Regulation, Neoplastic, Humans, Inhibitor of Differentiation Protein 2, Molecular Sequence Data, Neoplasms, Oxides, Pancreatic Neoplasms, Protein Biosynthesis, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Stomach Neoplasms, Transcription, Genetic, Transforming Growth Factor beta, Up-Regulation.
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Does upregulation of ID2 antagonize arsenic trioxide-induced antitumor effects in cancer cells? Context: Arsenic trioxide (ATO) strongly induces apoptosis and differentiation in acute promyelocytic leukemia, and induces cell cycle arrest in most solid tumors. Although many signaling pathways are involved in its antitumor mechanism, a detailed investigation of the transforming growth factor beta-bone morphogenetic protein signaling pathway has not been performed. A microarray containing 113 genes associated with the pathway was used to screen important molecules that participate in the antitumor effects of ATO. The expression levels of the inhibitors of DNA binding-2 (ID2) in 4 different types of cancer cells were determined by quantitative reverse transcription PCR and Western blotting. Human esophageal squamous cell carcinoma cell line Eca109 and pancreatic carcinoma cell line BxPC3 cells were transfected with siRNAs targeting ID2 and scrambled control siRNA. Cell proliferation was evaluated by methyl thiazolyl tetrazolium assay. Eighteen upregulated and 12 downregulated genes were identified. After verification at the transcriptional and translational levels in 4 different cancer cells, ID2 was identified as an ATO antitumor-associated protein. In addition, specific silencing of ID2 could enhance ATO-induced cell proliferation inhibition in cancer cells.
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A combination of ATO and ID2-targeted agents may have considerable therapeutic benefits in cancers. Final Decision: yes