Yao Huiping, Chen Rui, Yang Yongxiu, Jiang Juan
Department of Gynecology and Obstetrics, Gansu Key Laboratory of Gynecological Oncology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China.
Department of Gynecology, East Hospital Affiliated to Tongji University, Shanghai, 200120, China.
Reprod Sci. 2021 Mar;28(3):736-744. doi: 10.1007/s43032-020-00366-5. Epub 2020 Nov 6.
Ovarian cancer (OC) is a kind of common gynecological malignancy around the world. Mounting literatures have confirmed the implication of lncRNAs in the development of various cancers. Long non-coding RNA (LncRNA) BBOX1-AS1 has not been reported in most cancer types including OC. Presently, we aimed at exploring the function and regulatory mechanism of BBOX1-AS1 in OC. As a result, we demonstrated the extremely high BBOX1-AS1 expression in OC tissues and cells. BBOX1-AS1 silence inhibited OC progression by suppressing cell proliferation and promoting cell apoptosis. Importantly, BBOX1-AS1 was verified to bind to miR-361-3p, which presented a low expression trend in OC cells. Subsequently, PODXL was testified as the downstream target of miR-361-3p. Of note, BBOX1-AS1 positively regulated PODXL through their competition in binding with miR-361-3p. Furthermore, miR-361-3p inhibition facilitated the growth of BBOX1-AS1-deficient OC cells, while such facilitating effect was then counteracted in response to PODXL depletion. All the results above explained that BBOX1-AS1 was overexpressed in OC and that BBOX1-AS1 caused carcinogenic influences on OC cell growth via miR-361-3p/PODXL pathway, highlighting BBOX1-AS1 as a novel potential target for OC treatment.
卵巢癌（OC）是一种全球常见的妇科恶性肿瘤。越来越多的文献证实了长链非编码RNA（lncRNAs）在各种癌症发生发展中的作用。包括OC在内的大多数癌症类型中尚未见关于长链非编码RNA（LncRNA）BBOX1-AS1的报道。目前，我们旨在探讨BBOX1-AS1在OC中的功能及调控机制。结果显示，我们证实了BBOX1-AS1在OC组织和细胞中表达极高。BBOX1-AS1沉默通过抑制细胞增殖和促进细胞凋亡来抑制OC进展。重要的是，证实BBOX1-AS1与miR-361-3p结合，miR-361-3p在OC细胞中呈低表达趋势。随后，证实PODXL是miR-361-3p的下游靶点。值得注意的是，BBOX1-AS1通过与miR-361-3p竞争结合而正向调控PODXL。此外，抑制miR-361-3p可促进BBOX1-AS1缺失的OC细胞生长，而PODXL缺失则可抵消这种促进作用。上述所有结果表明，BBOX1-AS1在OC中过表达，且BBOX1-AS1通过miR-361-3p/PODXL途径对OC细胞生长产生致癌影响，凸显BBOX1-AS1作为OC治疗新的潜在靶点的地位。
