Cervical cancer (CC) is the most common malignant tumor in gynecology, and metastasis is an important cause of patient death. MiRNAs (microRNAs) have been found to play key roles in cervical cancer metastasis, but the effect of miR-362-3p in CC is unclear. This study aimed to investigate the role of miR-362-3p in cervical cancer migration and invasion. We compared the expression levels of miR-362-3p in cervical cancer tissues and adjacent normal cervical tissues. In CC tissues, miR-362-3p expression was significantly down-regulated, which is related to the cancer stage and patient survival. MiR-362-3p can effectively inhibit the migration and invasion of cervical cancer cells. The dual-luciferase reporter assay results showed that BCAP31 (B cell receptor associated protein 31) is a direct target protein of miR-362-3p. The results of the immunohistochemical examination of clinical tissue samples showed that BCAP31 was abnormally highly expressed in cervical cancer, which was positively correlated with the clinical stage. BCAP31 knockdown exerted similar effects as miR-362-3p overexpression. Further GSEA analysis showed that BCAP31 may participate in multiple biological processes, such as protein transport, metabolism, and organelle organization. Our results suggest that miR-362-3p inhibits migration and invasion via directly targeting BCAP31 in cervical cancer, and restoring miR-362-3p levels may be a new treatment strategy for cervical cancer in the future.

宫颈癌（CC）是妇科中最常见的恶性肿瘤，转移是导致患者死亡的重要原因。已发现miRNA（microRNA）在宫颈癌转移中起关键作用，但尚不清楚miR-362-3p在CC中的作用。这项研究旨在调查miR-362-3p在宫颈癌迁移和侵袭中的作用。我们比较了miR-362-3p在宫颈癌组织和邻近正常宫颈组织中的表达水平。在CC组织中，miR-362-3p表达显着下调，这与癌症分期和患者生存有关。MiR-362-3p可有效抑制子宫颈癌细胞的迁移和侵袭。双荧光素酶报告基因测定结果表明，BCAP31（B细胞受体相关蛋白31）是miR-362-3p的直接靶蛋白。临床组织标本的免疫组织化学检查结果表明，BCAP31在宫颈癌中异常高表达，与临床分期呈正相关。BCAP31敲除发挥与miR-362-3p过表达相似的作用。进一步的GSEA分析表明，BCAP31可能参与多种生物学过程，例如蛋白质转运，代谢和细胞器组织。我们的结果表明，miR-362-3p通过直接靶向BCAP31抑制子宫颈癌的迁移和侵袭，恢复miR-362-3p的水平可能是将来宫颈癌的新治疗策略。BCAP31敲除发挥与miR-362-3p过表达相似的作用。进一步的GSEA分析表明，BCAP31可能参与多种生物学过程，例如蛋白质转运，代谢和细胞器组织。我们的结果表明，miR-362-3p通过直接靶向BCAP31抑制子宫颈癌的迁移和侵袭，恢复miR-362-3p的水平可能是将来宫颈癌的新治疗策略。BCAP31敲除发挥与miR-362-3p过表达相似的作用。进一步的GSEA分析表明，BCAP31可能参与多种生物学过程，例如蛋白质转运，代谢和细胞器组织。我们的结果表明，miR-362-3p通过直接靶向BCAP31抑制子宫颈癌的迁移和侵袭，恢复miR-362-3p的水平可能是将来宫颈癌的新治疗策略。