The long noncoding RNA HOXA11 antisense induces tumor progression and stemness maintenance in cervical cancer
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Hee Jung Kim1,*, Kyung Jin Eoh1,2,*, Lee Kyung Kim1, Eun Ji Nam1, Sun Och Yoon3, Kun-Hong Kim4, Jae Kwan Lee5, Sang Wun Kim1, Young Tae Kim1
1Institute of Women's Life Medical Science, Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea
2Department of Obstetrics and Gynecology, Yonsei University Graduate School, Seoul, Korea
3Department of Pathology, Gangnam Severance Cancer Hospital, Yonsei University College of Medicine, Seoul, Korea
4Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Korea
5Department of Obstetrics and Gynecology, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Korea
*These authors have contributed equally to this work
Sang Wun Kim, email: [email protected]
Young Tae Kim, email: [email protected]
Keywords: HOXA11 antisense, long noncoding RNA, invasion, prognosis, cervical cancer
Received: August 08, 2016 Accepted: October 14, 2016 Published: October 25, 2016
Recent research has focused on the impact of long noncoding RNA (lncRNA) in cervical carcinogenesis. However, whether HOXA11 antisense (HOXA11-AS) is involved in cervical cancer remains to be elucidated. In the present study, we examined HOXA11-AS expression levels in cervical cancer patients and determined the relationships between HOXA11-AS expression and clinicopathological factors. We also investigated the bio-functional consequences of HOXA11-AS overexpression both in vitro and in vivo. HOXA11-AS expression was significantly greater in tissues from patients with cervical cancer than in control patients (P<0.001). Multivariate analysis showed that high HOXA11-AS was an independent prognosticator of overall survival (Hazard ratio=2.450, P=0.032). HOXA11-AS overexpression enhanced cell proliferation, migration, and tumor invasion in vitro, whereas HOXA11-AS knockdown inhibited these biologic aggressive features. These adverse changes were accompanied by characteristics of epithelial-mesenchymal transition (EMT). In vivo xenograft experiments using the siHOXA11-AS-transfected HeLa cells revealed that HOXA11-AS strongly induced tumor growth. Furthermore, we found that HOXA11-AS knockdown decreased cancer stemness and triggered the EMT program. In conclusion, HOXA11-AS overexpression correlated with poor survival in patients with cervical cancer. Thus, HOXA11-AS may be a pivotal target for exploring novel cervical cancer therapeutics.
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