目前发现，在非编码RNA中存在一种进化上极度保守的RNA(超保守非编码RNA,ucRNA)可调节miRNAs的生成，形成了新型的ncRNA-ncRNA互作网络，对恶性肿瘤转移生物学行为有重要影响。申请者前期发现uc.246在转移病人的乳腺癌原发灶中表达显著增高,并与其肺转移灶正相关。uc.246通过碱基互补能够结合pri-miR-203非茎环区形成局部RNA双链结构。结合前期研究基础，申请者推测uc.246可能通过RNA修饰/编辑依赖的机制抑制RNA结合蛋白DGCR8与pri-miR-203结合，从而抑制Drosha对pri-miR-203的切割而下调了miR-203-5p的表达，诱导乳腺癌细胞EMT，最终促进乳腺癌侵袭转移。本研究通过RNApulldown、RNA-Seq、RIP等分子生物学技术，探讨uc.246促进乳腺癌侵袭转移的分子机制，为乳腺癌侵袭转移提供新的诊断标记物及治疗靶点。

Recent studies have found that an evolutionarily extremely conserved RNA (super-conservative non-coding RNA, ucRNA) in non-coding RNA that can regulate the generation of miRNAs, forming a new type of ncRNA-ncRNA interaction network, which is of great importance to the biological behavior of malignant tumor metastasis. The applicant early found that the expression of uc.246 in primary breast cancer of metastatic patients was significantly increased, and it was positively correlated with lung metastases. uc.246 can bind to the non-stem loop region of pri-miR-203 through complementary base which forms a local RNA double-stranded structure. Based on the previous research, the applicant speculates that uc.246 may inhibit the combination of RNA-binding protein DGCR8 and pri-miR-203 through an RNA modification/edit-dependent mechanism, thereby inhibiting Drosha's cleavage of pri-miR-203 and downregulating the expression of miR-203-5p, which induces EMT of breast cancer cells and eventually promotes the invasion and metastasis of breast cancer. This study explores the molecular mechanism of uc.246 which promotes breast cancer invasion and metastasis through molecular biological techniques such as RNA pulldown、RNA-Seq and RIP, which provides new diagnostic markers and therapeutic targets for breast cancer invasion and metastasis.