Upregulation of LINC01503 promotes cervical cancer progression by targeting the miR-615-3p/CCND1 axis.
Upregulation of LINC01503 promotes cervical cancer progression by targeting the miR-615-3p/CCND1 axis.
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DOI：
10.7150/jca.54148
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发表时间：
2021
影响因子：
3.9
通讯作者：
Xi J
中科院分区：
文献类型：
--
作者：
Feng J;Gao FY;Li YY;Xiao XY;Xi J
越来越多的证据表明，长链非编码rna影响宫颈癌的进展，但LINC01503在该疾病发病机制中的确切功能尚不清楚。在这里，我们发现宫颈癌组织中LINC01503的水平较高。高表达的LINC01503与宫颈癌进展加快相关，表现为FIGO晚期、肿瘤细胞向淋巴结转移增加以及向更深的宫颈组织浸润。抑制LINC01503明显抑制肿瘤细胞的侵袭和增殖能力。在机制上，LINC01503被证明可以负向调节miR-615-3p在宫颈癌中的表达。CCND1被发现是miR-615-3p的靶标。挽救实验表明，抑制LINC01503抑制肿瘤细胞的侵袭和增殖能力，这一现象在抑制miR-615-3p或过表达CCND1后被逆转。总的来说，这些数据表明LINC01503通过与miR-615-3p/CCND1轴的相互作用增强宫颈癌细胞的进展。
Mounting evidence indicates that long non-coding RNAs influence the progression of cervical cancer, but the precise function of LINC01503 in the pathogenesis of the disease remains unknown. Here, we found higher levels of LINC01503 in cervical cancer tissues. High LINC01503 expression was associated with enhanced progression of cervical cancer as indicated by advanced FIGO stage, increased metastasis of tumor cells to lymph nodes, and invasion into deeper cervical tissues. LINC01503 inhibition markedly suppressed the invasion and proliferative ability of tumor cells. Mechanistically, LINC01503 was demonstrated to negatively modulate the expression of miR-615-3p in cervical cancer. CCND1 was found to be a target of miR-615-3p. Rescue experiments indicated that LINC01503 inhibition suppressed the invasion and proliferative ability of the tumor cells, a phenomenon that was reversed following miR-615-3p inhibition or CCND1 overexpression. Collectively, these data indicate that LINC01503 enhances the progression of cervical cancer cells via interaction with miR-615-3p/CCND1 axis.
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