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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: Animals, Apoptosis, Cell Line, Tumor, Cyclin D1, Humans, Inhibitor of Apoptosis Proteins, Laryngeal Neoplasms, Mice, Mice, Nude, Microtubule-Associated Proteins, Neoplasm Proteins, Neoplasm Transplantation, Proto-Oncogene Proteins c-bcl-2, RNA Interference, RNA, Messenger, RNA, Small Interfering, STAT3 Transcription Factor, Survivin.
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Does knockdown of Stat3 expression using RNAi inhibit growth of laryngeal tumors in vivo? Context: To study the effect of pSilencer1.0-U6-siRNA-stat3 on the growth of human laryngeal tumors in nude mice. Hep2 cells were transplanted into nude mice, then at the time of tumor formation, growth rates were observed. After the tumor formed, pSilencer1.0-U6-siRNA-stat3 was injected. Tumor volumes were calculated, and growth curves were plotted. Representative histological sections were taken from mice bearing transplantation tumors in both treated and control groups, and stat3, pTyr-stat3, Bcl-2, cyclin D1, and survivin expression were detected by Western blotting. survivin mRNA levels were detected by Northern blotting, hematoxylin and eosin staining and terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling (TUNEL) assay to confirm the apoptosis of tumors. In nude mice, pSilencer1.0-U6-siRNA-stat3 significantly suppressed the growth of tumors compared with controls (P<0.01). It suppressed stat3 expression, and downregulated BcL2, cyclin D1, and survivin expression within the tumor. This significantly induced apoptosis of the tumors.
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pSilencer1.0-U6-siRNA-stat3 was able to inhibit the growth of transplanted human laryngeal tumors in nude mice and induce apoptosis. Final Decision: yes