HPV-type-specific response of cervical cancer cells to cisplatin after silencing replication licensing factor MCM4

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• 作者：Mitali Das ; Shyam Babu Prasad ; Suresh Singh Yadav ; Arusha Modi…
• 关键词：Cervical cancer ; HPV status ; MCM4 ; RNA interference ; Cisplatin ; Chromosomal instability
• 刊名：Tumor Biology
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：36
• 期：12
• 页码：9987-9994
• 全文大小：1,500 KB
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• 作者单位：Mitali Das (1)
  Shyam Babu Prasad (1) (4)
  Suresh Singh Yadav (1)
  Arusha Modi (1)
  Sunita Singh (2)
  Satyajit Pradhan (3)
  Gopeshwar Narayan (1)
  
  1. Cancer Genetics Laboratory, Department of Molecular and Human Genetics, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India
  4. Division of Molecular Oncology, Institute of Cytology and Preventive Oncology, I-7, Sector-39, Noida, 201 301, India
  2. Department of Zoology, Mahila Mahavidyalaya, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India
  3. Department of Radiotherapy and Radiation Medicine, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India
  
• 刊物主题：Cancer Research;
• 出版者：Springer Netherlands
• ISSN：1423-0380

文摘

Minichoromosome maintenance (MCM) proteins play key role in cell cycle progression by licensing DNA replication only once per cell cycle. These proteins are found to be overexpressed in cervical cancer cells. In this study, we depleted MCM4, one of the MCM 2–7 complex components by RNA interference (RNAi) in four cervical cancer cell lines. The four cell lines were selected on the basis of their human papillomavirus (HPV) infection: HPV16-positive SiHa, HPV18-positive ME-180, HPV16- and HPV18-positive CaSki, and HPV-negative C-33A. The MCM4-deficient cells irrespective of their HPV status grow for several generations and maintain regular cell cycle. We did not find any evidence of augmented response to a short-term (48 h) cisplatin treatment in these MCM4-deficient cells. However, MCM4−/HPV16+ SiHa cells cannot withstand a prolonged treatment (up to 5 days) of even a sublethal dosage of cisplatin. They show increased chromosomal instability compared to their control counterparts. On the other hand, MCM4-deficient CaSki cells (both HPV16+ and 18+) remain resistant to a prolonged exposure to cisplatin. Our study indicates that cervical cancer cells may be using excess MCMs as a backup for replicative stress; however, its regulatory mechanism is dependent on the HPV status of the cells. Keywords Cervical cancer HPV status MCM4 RNA interference Cisplatin Chromosomal instability