[Influence on cell proliferation by small interfering RNA of Cyclin Y expression in laryngeal cancer cells].

Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi

Beijing Key Laboratory for Pediatric Otolaryngology, Head and Neck Science, Beijing Pediatric Research Institute,Beijing Children's Hospital, Capital Medical University, Beijing 100045, China.

Published: September 2013

AI Article Synopsis

  • - The study focused on how reducing Cyclin Y (CCNY) expression using lentivirus affects laryngeal cancer cell growth in lab settings.
  • - Hep-2 laryngeal cancer cells were divided into two groups: one receiving a control virus and the other receiving a virus that suppressed CCNY, leading to a significant reduction in CCNY levels and cell viability.
  • - Results showed that the CCNY knockdown led to a 60% decrease in the number of colonies formed by cancer cells, indicating that targeting CCNY could be a potential strategy for treating laryngeal cancer.

Article Abstract

Objective: The effects of lentivirus-mediated suppression of Cyclin Y (CCNY) expression on the proliferation of laryngeal cancer cells were investigated in vitro.

Methods: The lentivirus vectors containing a small hairpin RNA (shRNA) to target CCNY were constructed.Hep-2 cells were divided into the following two experimental groups:the negative control group (control lentivirus infected cells) and CCNY knockdown group (CCNY shRNA-expressing lentivirus infected cells). After Hep-2 cells were infected, Real-time PCR was used to measure CCNY expression. The influence of CCNY on the proliferation of laryngeal cancer cells were assessed using MTT and colony formation experiments.Each experiment was performed in triplicate and repeated three times.

Results: Lentiviruses expressing shRNA against CCNY were constructed and Hep-2 cells were infected with above mentioned lentivirus at MOI (Multiplicity of infection) of 120.Real-time PCR analysis showed that the mRNA expression of CCNY in Hep-2 cells in the knockdown group was significantly decreased (P < 0.05); the mRNA level of CCNY was 75.3% lower in the si-CCNY group than in the si-CTRL group. After 5 days of lentiviral infection, the cell viability was significantly lower in cells infected with the CCNY-shRNA lentivirus compared to cells infected with the control lentivirus following a 6-day incubation. The colony number was decreased by 60% in Hep-2 cells infected with the CCNY-shRNA-lentivirus infected cells following a 10-day incubation.

Conclusions: The results suggested that lentivirus-mediated downregulation of CCNY expression decreased the proliferation and growth potency of laryngeal cancer cells.Lentiviruses delivering shRNA against CCNY may be a promising tool for laryngeal cancer therapy.

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