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Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro

BACKGROUND: The prognosis of oral squamous cell carcinoma is very poor due to local recurrence and metastasis. This study explores the molecular events involved in oral carcinoma with the goal of developing novel therapeutic strategies. The mitotic spindle is a complex mechanical apparatus required...

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Autores principales: Zhang, Bin, Li, Ke Yi, Chen, Hai Ying, Pan, Shao Dong, Jiang, Li Cheng, Wu, Ya Ping, Liu, Shu Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765658/
https://www.ncbi.nlm.nih.gov/pubmed/23962337
http://dx.doi.org/10.1186/1475-2867-13-83
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author Zhang, Bin
Li, Ke Yi
Chen, Hai Ying
Pan, Shao Dong
Jiang, Li Cheng
Wu, Ya Ping
Liu, Shu Wei
author_facet Zhang, Bin
Li, Ke Yi
Chen, Hai Ying
Pan, Shao Dong
Jiang, Li Cheng
Wu, Ya Ping
Liu, Shu Wei
author_sort Zhang, Bin
collection PubMed
description BACKGROUND: The prognosis of oral squamous cell carcinoma is very poor due to local recurrence and metastasis. This study explores the molecular events involved in oral carcinoma with the goal of developing novel therapeutic strategies. The mitotic spindle is a complex mechanical apparatus required for the accurate segregation of sister chromosomes during mitosis. Spindle and kinetochore associated complex subunit 1 (SKA1) is a microtubule-binding subcomplex of the outer kinetochore that is essential for proper chromosome segregation. In recent years, much attention has been focused on determining how SKA proteins interact with each other, as well as their biological role in cancer cells. However, the precise role of SKA1 in oral carcinoma remains unknown. METHODS: In order to investigate the role of SKA1 in oral cancer, we employed lentivirus-mediated shRNA to silence SKA1 expression in the CAL-27 human oral adenosquamous carcinoma cell line. RESULTS: Depletion of SKA1 in CAL-27 cells significantly decreased cell proliferation, as determined by MTT and colony formation assays. These results strongly demonstrate that reduced SKA1 protein levels may cause inhibition of tumor formation. The shRNA-mediated depletion of SKA1 also led to G2/M phase cell cycle arrest and apoptosis. CONCLUSION: This is the first report to show that SKA1 plays an important role in the progression of oral adenosqamous carcinoma. Thus, silencing of SKA1 by RNAi might be a potential therapy for this disease.
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spelling pubmed-37656582013-09-08 Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro Zhang, Bin Li, Ke Yi Chen, Hai Ying Pan, Shao Dong Jiang, Li Cheng Wu, Ya Ping Liu, Shu Wei Cancer Cell Int Primary Research BACKGROUND: The prognosis of oral squamous cell carcinoma is very poor due to local recurrence and metastasis. This study explores the molecular events involved in oral carcinoma with the goal of developing novel therapeutic strategies. The mitotic spindle is a complex mechanical apparatus required for the accurate segregation of sister chromosomes during mitosis. Spindle and kinetochore associated complex subunit 1 (SKA1) is a microtubule-binding subcomplex of the outer kinetochore that is essential for proper chromosome segregation. In recent years, much attention has been focused on determining how SKA proteins interact with each other, as well as their biological role in cancer cells. However, the precise role of SKA1 in oral carcinoma remains unknown. METHODS: In order to investigate the role of SKA1 in oral cancer, we employed lentivirus-mediated shRNA to silence SKA1 expression in the CAL-27 human oral adenosquamous carcinoma cell line. RESULTS: Depletion of SKA1 in CAL-27 cells significantly decreased cell proliferation, as determined by MTT and colony formation assays. These results strongly demonstrate that reduced SKA1 protein levels may cause inhibition of tumor formation. The shRNA-mediated depletion of SKA1 also led to G2/M phase cell cycle arrest and apoptosis. CONCLUSION: This is the first report to show that SKA1 plays an important role in the progression of oral adenosqamous carcinoma. Thus, silencing of SKA1 by RNAi might be a potential therapy for this disease. BioMed Central 2013-08-20 /pmc/articles/PMC3765658/ /pubmed/23962337 http://dx.doi.org/10.1186/1475-2867-13-83 Text en Copyright © 2013 Zhang et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Primary Research
Zhang, Bin
Li, Ke Yi
Chen, Hai Ying
Pan, Shao Dong
Jiang, Li Cheng
Wu, Ya Ping
Liu, Shu Wei
Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro
title Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro
title_full Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro
title_fullStr Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro
title_full_unstemmed Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro
title_short Spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma CAL-27 cells in vitro
title_sort spindle and kinetochore associated complex subunit 1 regulates the proliferation of oral adenosquamous carcinoma cal-27 cells in vitro
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765658/
https://www.ncbi.nlm.nih.gov/pubmed/23962337
http://dx.doi.org/10.1186/1475-2867-13-83
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