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HPV-type-specific response of cervical cancer cells to cisplatin after silencing replication licensing factor MCM4.
Das, Mitali; Prasad, Shyam Babu; Yadav, Suresh Singh; Modi, Arusha; Singh, Sunita; Pradhan, Satyajit; Narayan, Gopeshwar.
Afiliación
  • Das M; Cancer Genetics Laboratory, Department of Molecular and Human Genetics, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India.
  • Prasad SB; Cancer Genetics Laboratory, Department of Molecular and Human Genetics, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India.
  • Yadav SS; Division of Molecular Oncology, Institute of Cytology and Preventive Oncology, I-7, Sector-39, Noida, 201 301, India.
  • Modi A; Cancer Genetics Laboratory, Department of Molecular and Human Genetics, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India.
  • Singh S; Cancer Genetics Laboratory, Department of Molecular and Human Genetics, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India.
  • Pradhan S; Department of Zoology, Mahila Mahavidyalaya, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India.
  • Narayan G; Department of Radiotherapy and Radiation Medicine, Banaras Hindu University, Varanasi, 221 005, Uttar Pradesh, India.
Tumour Biol ; 36(12): 9987-94, 2015 Dec.
Article en En | MEDLINE | ID: mdl-26188903
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias del Cuello Uterino / Cisplatino / Resistencia a Antineoplásicos / Componente 4 del Complejo de Mantenimiento de Minicromosoma Límite: Female / Humans Idioma: En Revista: Tumour Biol Asunto de la revista: NEOPLASIAS Año: 2015 Tipo del documento: Article País de afiliación: India Pais de publicación: Países Bajos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias del Cuello Uterino / Cisplatino / Resistencia a Antineoplásicos / Componente 4 del Complejo de Mantenimiento de Minicromosoma Límite: Female / Humans Idioma: En Revista: Tumour Biol Asunto de la revista: NEOPLASIAS Año: 2015 Tipo del documento: Article País de afiliación: India Pais de publicación: Países Bajos