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

Wang,Jue; Li,Hui; Zhang,Cuiying; Xue,Liying; Cai,Zhihui

doi:10.3892/ol.2019.10425

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

Authors:
- Jue Wang
- Hui Li
- Cuiying Zhang
- Liying Xue
- Zhihui Cai
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Affiliations: Department of Oncology, Inner Mongolia People's Hospital, Hohhot, Inner Mongolia 010017, P.R. China
Published online on: May 31, 2019 https://doi.org/10.3892/ol.2019.10425
Pages: 1491-1496
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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.

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