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. 2017 Oct 15;9(10):4545-4552.
eCollection 2017.

Knockdown of HOXA-AS2 suppresses proliferation and induces apoptosis in colorectal cancer

Gangling Tong  1 , Xuan Wu  1 , Boran Cheng  1 , Liang Li  2 , Xi Li  3 , Zhu Li  1 , Qiaohong Nong  1 , Xiaoqiu Chen  1 , Yajie Liu  1 , Shubin Wang  1
Affiliations

Knockdown of HOXA-AS2 suppresses proliferation and induces apoptosis in colorectal cancer

Gangling Tong et al. Am J Transl Res. .

Abstract

Colorectal cancer (CRC) remains one of the most common cancers worldwide. Increasing evidence indicates that long non-coding RNAs (lncRNAs) regulate diverse cellular processes, including cell growth, differentiation, apoptosis, and cancer progression. However, the function of lncRNAs in the progression of CRC remains largely unknown. Here, we reported that HOXA cluster antisense RNA2 (HOXA-AS2) was upregulated in CRC. Increased HOXA-AS2 expression in CRC was associated with larger tumor size and higher clinical stage. In vitro experiments revealed that HOXA-AS2 knockdown significantly inhibited CRC cell proliferation by causing G1 arrest and promoting apoptosis, whereas HOXA-AS2 overexpression promoted cell proliferation. Further functional assays indicated that HOXA-AS2 overexpression significantly promoted cell migration and invasion by regulating the epithelial-mesenchymal transition (EMT). In conclusion, our study identifies HOXA-AS2C as a potential biomarker in CRC.

Keywords: CRC; EMT; HOXA-AS2C; LncRNA; metastasis.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
A. HOXA-AS2 was detected in CRC tissues and adjacent noncancerous tissues by qRT-PCR. B. qRT-PCR showing expression level of HOXA-AS2 in CRC cell lines. C. We employed siRNA to enhance efficiency of HOXA-AS2 knockdown in CRC cell lines. D. We employed expressing plasmid to enhance efficiency of HOXA-AS2 overexpression in CRC cell lines.
Figure 2
Figure 2
A. CCK8 assay showing knockdown of HOXA-AS2 inhibited cell proliferation of HCT116 cells. B. CCK8 assay showing overexpreesion of HOXA-AS2 promoted cell proliferation of LoVo cells. C. Colony formation assay showing knockdown of HOXA-AS2 inhibited cell proliferation of HCT116 cells. D. Colony formation assay showing overexpreesion of HOXA-AS2 promoted cell proliferation of LoVo cells.
Figure 3
Figure 3
A. HCT116 cells transfected with si-HOXA-AS2 all had cell-cycle arrest at the G1-G0 phase compared with cells transfected with si-NC. B. Overexpression of HOXA-AS2 in LoVo cells led to a increase in the number of cells in the S-phase and an decrease in the percentage of cells in the G0/G1 phase. C. Knockdown of HOXA-AS2 induced cell apoptosis of HCT116 cells. D. Overexpression of HOXA-AS2 cell suppressed apoptosis of LoVo cells.
Figure 4
Figure 4
A. Inhibition of Migration and Invasion of HCT116 cells by HOXA-AS2 siRNA. B. Overexpreesion of HOXA-AS2 promoted Migration and Invasion of LoVo cells. C. Knockdown of HOXA-AS2 reverses EMT in HCT116 cells. D. Overexpreesion of HOXA-AS2 induces EMT in LoVo cells.
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