MicroRNA-29a promotes colorectal cancer metastasis by regulating matrix metalloproteinase 2 and E-cadherin via KLF4

التفاصيل البيبلوغرافية
العنوان: MicroRNA-29a promotes colorectal cancer metastasis by regulating matrix metalloproteinase 2 and E-cadherin via KLF4
المؤلفون: Y Leng, Peng Du, Yunxiang Zhu, Chen-Ying Liu, Wei Tang, Xiang Zhou, Long Cui, Wei Chen, Shenglin Huang, Jiuhong Kang, Chenlin Song, Jihong Fu, Jun Gao, S Zhu, Guanghui Wang, Yingbin Liu
المصدر: British Journal of Cancer
بيانات النشر: Springer Science and Business Media LLC, 2013.
سنة النشر: 2013
مصطلحات موضوعية: Male, Oncology, Cancer Research, medicine.medical_specialty, MMP2, Kruppel-Like Transcription Factors, Mice, Nude, colorectal cancer, Biology, Metastasis, Kruppel-Like Factor 4, Mice, Western blot, Cell Movement, Cell Line, Tumor, Internal medicine, microRNA, medicine, metastasis, Animals, Humans, Neoplasm Invasiveness, Neoplasm Metastasis, Molecular Diagnostics, Regulation of gene expression, Gene knockdown, medicine.diagnostic_test, miR-29a, Cancer, Cadherins, HCT116 Cells, Prognosis, medicine.disease, KLF4, Gene Expression Regulation, Neoplastic, MicroRNAs, HEK293 Cells, Cancer research, Matrix Metalloproteinase 2, Colorectal Neoplasms
الوصف: Background: Growing evidence suggests that miR-29a has an important role in regulating tumourigenesis and development of various types of cancer. However, the role and the underlying mechanism of miR-29a in colorectal cancer (CRC) remain largely unknown. Methods: MiR-29a targeted gene was identified by the luciferase assay and western blot. MiR-29a function was analysed by invasion assays and the orthotopic transplantation mouse model. The miR-29a pathway was assayed by real-time PCR, western blot and chip analysis. Results: KLF4 was identified as a direct target gene of miR-29a. MiR-29a promoted CRC cell invasion, which was blocked by re-expression of KLF4. In addition, MMP2 was identified as a novel direct target of KLF4. Both miR-29a overexpression and KLF4 knockdown promoted MMP2 expression but inhibited E-cadherin expression. Furthermore, clinical data indicated that both miR-29a high expression and KLF4 mRNA low expression were associated with metastasis and poor prognosis in CRC patients, and KLF4 protein expression was inversely correlated with MMP2 but positively correlated with E-cad protein expression. Conclusion: Increased expression of miR-29a promoted CRC metastasis by regulating MMP2/E-cad through direct targeting KLF4, which highlights the potential of the miR-29a inhibitor as a novel agent against CRC metastasis.
تدمد: 1532-1827
0007-0920
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::20bb3e94c718f4a570a29530c1393344Test
https://doi.org/10.1038/bjc.2013.724Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....20bb3e94c718f4a570a29530c1393344
قاعدة البيانات: OpenAIRE