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. 2019 Jun;19(6):5275-5280.
doi: 10.3892/mmr.2019.10191. Epub 2019 Apr 25.

LINC01638 silencing inhibits cancer cell proliferation in colorectal adenocarcinoma through interaction with RUNX2

Wenying Zhuo  1 , Dengdi Hu  1 , Xihua Chen  1 , Tian Zhang  1
Affiliations

LINC01638 silencing inhibits cancer cell proliferation in colorectal adenocarcinoma through interaction with RUNX2

Wenying Zhuo et al. Mol Med Rep. 2019 Jun.

Retraction in

Abstract

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.

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Figures

Figure 1.
Figure 1.
LINC01638 in plasma is upregulated in colorectal adenocarcinoma patients an is affected by tumor size (*P<0.05).
Figure 2.
Figure 2.
LINC01638 in plasma of colorectal adenocarcinoma patients is not affected by tumor distant metastasis.
Figure 3.
Figure 3.
Plasma RUNX2 mRNA levels are upregulated in colorectal adenocarcinoma patients and are positively correlated with the levels of lncRNA LINC01638. (A) Plasma RUNX2 mRNA levels were upregulated in colorectal adenocarcinoma patients compared to healthy controls (*P<0.05). Plasma levels of RUNX2 mRNA and lncRNA LINC01638 were positively correlated in (B) colorectal adenocarcinoma patients but not in (C) healthy controls.
Figure 4.
Figure 4.
Plasma LINC01638 has diagnostic potential for early stage colorectal adenocarcinoma.
Figure 5.
Figure 5.
LINC01638 shRNA silencing mediates downreguatin of RUNX2 in cells of WiDr and HT-29 human colorectal adenocarcinoma cell lines. (A) LINC01638 shRNA silencing led to significantly downregulated expression of RUNX2 protein in cells of WiDr and HT-29 human colorectal adenocarcinoma cell lines, while (B) RUNX2 overexpression failed to significanly affect the expression of LINC01638 (*P<0.05).
Figure 6.
Figure 6.
LINC01638 shRNA inhibits cancer cell proliferation possibly through RUNX2. LINC01638 shRNA silencing (shRNA) significantly inhibited, while RUNX2 overexpression (RUNX2) significantly promoted the proliferation of cells of both (A) WiDr and (B) HT-29 human colorectal adenocarcinoma cell lines. In addition, RUNX2 overexpression partially reversed the advese effect of LINC01638 shRNA silencing on cancer cell proliferation (*P<0.05).
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