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Knockdown of ST6Gal-I increases cisplatin sensitivity in cervical cancer cells

BACKGROUND: Sialyltransferase I (ST6Gal-I) is an enzyme involved in tumor metastasis that processes sialic acid precursors into their mature form, enabling them to regulate gene expression. However, the effect of ST6Gal-I on the biological behavior of cancer cells remain unclear. This study was the...

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Detalles Bibliográficos
Autores principales: Zhang, Xiaopeng, Pan, Chunchen, Zhou, Lei, Cai, Zhaogen, Zhao, Shufang, Yu, Donghong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5162090/
https://www.ncbi.nlm.nih.gov/pubmed/27986075
http://dx.doi.org/10.1186/s12885-016-2981-y
Descripción
Sumario:BACKGROUND: Sialyltransferase I (ST6Gal-I) is an enzyme involved in tumor metastasis that processes sialic acid precursors into their mature form, enabling them to regulate gene expression. However, the effect of ST6Gal-I on the biological behavior of cancer cells remain unclear. This study was the first to demonstrate the influence of ST6Gal-I on cisplatin sensitivity in cervical cancer cells. METHODS: Knockdown of ST6Gal-I was performed by shRNA and HeLa cells combination with cisplatin were tested. RESULTS: We showed that down-regulation of ST6Gal-I promoted cell apoptosis and inhibited proliferation and invasion in cervical cancer cells. Knockdown of ST6Gal-I by RNA interference increased the sensitivity of HeLa cells to cisplatin in vitro, and reduced tumor volume and suppressed subcutaneous tumor growth in response to cisplatin treatment in a xenograft mouse model in vivo. CONCLUSIONS: The results provide new information that ST6Gal-I plays an important role in several biological or pathological processes including drug resistance in cervical cancer and may be a potential therapeutic target to improve the response to chemotherapy in cervical cancer patients. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12885-016-2981-y) contains supplementary material, which is available to authorized users.