LINC01638 silencing inhibits cancer cell proliferation in colorectal adenocarcinoma through interaction with RUNX2
- Wenying Zhuo
- Dengdi Hu
- Xihua Chen
- Tian Zhang
Affiliations: Department of General Surgery, Cixi People's Hospital, Cixi, Zhejiang 315300, P.R. China
- Published online on: April 25, 2019 https://doi.org/10.3892/mmr.2019.10191
Copyright: © Zhuo
et al. This is an open access article distributed under the
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Commons Attribution License.
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lncRNA LINC01638 has been revealed to play an oncogenic role in triple negative breast cancer. The present study was carried out to investigate the involvement of LINC01638 in colorectal adenocarcinoma. In the present study it was observed that LINC01638 in plasma was upregulated in colorectal adenocarcinoma patients compared to healthy controls. Plasma levels of LINC01638 were affected by tumor size but not by distant metastasis. Plasma levels of Runt‑related transcription factor 2 (RUNX2) were also higher in colorectal adenocarcinoma patients than in healthy controls, and were positively correlated with plasma levels of LINC01638 in colorectal adenocarcinoma patients but not in healthy controls. ROC curve analysis revealed that upregulation of LINC01638 distinguished colorectal adenocarcinoma at stage I and II from healthy controls. LINC01638 shRNA knockdown led to RUNX2 downregulation, while RUNX2 overexpression exhibited no significant effects on LINC01638. LINC01638 shRNA knockdown inhibited and RUNX2 overexpression promoted the proliferation of colorectal adenocarcinoma cells. RUNX2 overexpression attenuated the effects of LINC01638 shRNA knockdown on cancer cell proliferation. Therefore, lncRNA LINC01638 silencing may inhibit cancer cell proliferation in colorectal adenocarcinoma through its interaction with RUNX2.