LncRNA FOXD2-AS1 accelerates the progression of cervical cancer via downregulating CDX1

D.-Z. Chen, T.-F. Wang, W.-C. Dai, X. Xu, P.-F. Chen

Department of Obstetrics and Gynecology, Fujian Medical University Union Hospital, Fujian, China. fenfangsiji_cpf@163.com

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• Oncology

OBJECTIVE: To uncover the role of FOXD2-AS1 in aggravating the progression of cervical cancer (CC) by negatively regulating caudal-related homeobox 1 (CDX1).

MATERIALS AND METHODS: FOXD2-AS1 levels in CC tissues with different tumor sizes and tumor staging were detected. Meanwhile, FOXD2-AS1 levels in CC patients either with vascular invasion, lymphatic metastasis or not were detected. Survival analysis on CC patients expressing high level or low level of FOXD2-AS1 was conducted by introducing the Kaplan-Meier method. After the silence of FOXD2-AS1, proliferative changes in SiHa and HeLa cells were assessed through cell counting kit-8 (CCK-8) and 5-Ethynyl-2’-deoxyuridine (EdU) assay. Subcellular distribution of FOXD2-AS1 in CC cells was analyzed. Next, CDX1 level in CC tissues and para-tumor tissues was determined. The potential correlation between CDX1 level and FOXD2-AS1 level was evaluated by the linear regression analysis. At last, the regulatory effects of FOXD2-AS1/CDX1 on the proliferative ability of CC were examined.

RESULTS: FOXD2-AS1 was upregulated in CC tissues relative to those of para-tumor tissues, especially in those with larger tumor size and advanced tumor staging. Its level was not correlated to vascular invasion and lymphatic metastasis of CC. CC patients expressing a high level of FOXD2-AS1 suffered worse prognosis than those with low level. The silence of FOXD2-AS1 attenuated SiHa and HeLa cells to proliferate. FOXD2-AS1 was found to be mainly enriched in the nucleus. CDX1 was downregulated in CC tissues and its level was negatively regulated by FOXD2-AS1. The silence of CDX1 could reverse the regulatory effect of FOXD2-AS1 on the proliferative ability of CC cells.

CONCLUSIONS: FOXD2-AS1 is upregulated in CC and its high level predicts a poor prognosis of CC patients. It accelerates the malignant progression of CC via negatively regulating CDX1 level.

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