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Cervical carcinoma high-expressed long non-coding RNA 1 may promote growth of colon adenocarcinoma through interleukin-17A

Cervical carcinoma high-expressed long non-coding RNA 1 (CCHE1) has been demonstrated to promote several different types of cancer; however, the involvement of CCHE1 in other types of cancer remains unknown. In the present study, the expression levels of CCHE1 and interleukin (IL)-17A were increased...

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Detalles Bibliográficos
Autores principales: Wang, Jue, Li, Hui, Zhang, Cuiying, Xue, Liying, Cai, Zhihui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6607382/
https://www.ncbi.nlm.nih.gov/pubmed/31423215
http://dx.doi.org/10.3892/ol.2019.10425
Descripción
Sumario:Cervical carcinoma high-expressed long non-coding RNA 1 (CCHE1) has been demonstrated to promote several different types of cancer; however, the involvement of CCHE1 in other types of cancer remains unknown. In the present study, the expression levels of CCHE1 and interleukin (IL)-17A were increased in the plasma of patients with metastatic and non-metastatic colon adenocarcinoma (MC and NMC, respectively) compared with the healthy controls. There was no significant difference in the plasma expression levels of CCHE1 and IL-17A in patients with MC compared with patients with NMC. The plasma expression levels of CCHE1 and IL-17A were positively associated with the primary tumor diameter. A significant correlation as demonstrated between the serum levels of CCHE1 and IL-17A in patients with colon adenocarcinoma, but not in the healthy controls. CCHE1 and IL-17A overexpression promoted colon adenocarcinoma cell proliferation. Transfection of small interfering RNA against IL-17A partially reversed the effects of CCHE1 overexpression on cancer cell proliferation. Upregulation of IL-17A was observed after CCHE1 overexpression, while IL-17A overexpression did not significantly change the expression level of CCHE1. Therefore, CCHE1 may promote growth of colon adenocarcinoma through interactions with IL-17A.