MicroRNA-187 inhibits tumor growth and invasion by directly targeting CD276 in colorectal cancer

نویسندگان

  • Zheng-Shi Wang
  • Ming Zhong
  • Yu-Hai Bian
  • Yi-Fei Mu
  • Shao-Lan Qin
  • Min-Hao Yu
  • Jun Qin
چکیده

Aberrantly expressed microRNAs contribute to the initiation and progression of human cancers. However, the underlying functions of microRNA-187 (miR-187) in colorectal cancer (CRC) remain largely unexplored. Here, we demonstrated that miR-187 was significantly down-regulated in CRC tissues and cell lines compared to their normal counterparts. By Kaplan-Meier analysis, we revealed that decreased miR-187 expression was closely associated with shorter overall survival and relapse-free survival of patients with CRC. By gain- and loss-of-function studies, we showed that miR-187 remarkably suppressed CRC cell proliferation, migration, invasion, and promoted cell apoptosis. Furthermore, bioinformatics analysis and luciferase reporter assay identified that CD276 was the direct functional target of miR-187 in CRC. Genetic silencing of CD276 recapitulated similar phenotype as observed in over-expression of miR-187, and restoration of CD276 completely rescued the inhibitory effect of miR-187 in CRC cells. Taken together, our study implied the essential roles of miR-187 in suppressing CRC progression, and a novel link between miR-187 and CD276 in CRC.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

miR-506 inhibits cell proliferation and invasion by targeting TET family in colorectal cancer

Objective(s): Ten-eleven translocation (TET) family members have been shown to be involved in the development of many tumors. However, the biological role of the TET family and its mechanism of action in colorectal carcinogenesis and progression remain poorly understood. Materials and Methods:We measured the expression levels of TET family members in colorectal cancer (CRC) specimens, in the c...

متن کامل

نقش microRNA-21 در سرطان کولورکتال و قابلیت آن به عنوان یک بیومارکر پیش بینی کننده، تشخیصی و پیش آگهی: مقاله مروری

Colorectal cancer (CRC) is one of the most common types of cancers worldwide. Despite the improved therapeutic and diagnostic strategies and screening programs, morbidity and mortality of CRC is still considerable. Currently, most common approaches for diagnosis of CRC are colonoscopy and fecal occult blood test (FOBT). Because of the invasive nature of colonoscopy and low sensitivity of FOBT, ...

متن کامل

Colorectal Cancer Migration and Invasion Initiated by microRNA-106a

MicroRNAs have been implicated in the regulation of several cellular signaling pathways of colorectal cancer (CRC) cells. Although emerging evidence proves that microRNA (miR)-106a is expressed highly in primary tumor and stool samples of CRC patients; whether or not miR-106a mediates cancer metastasis is unknown. We show here that miR-106a is highly expressed in metastatic CRC cells, and regul...

متن کامل

MicroRNA-339-5p inhibits colorectal tumorigenesis through regulation of the MDM2/p53 signaling

Tumor suppressor p53 plays a central role in tumor suppression. To ensure its proper function, the levels and activity of p53 are under a tight regulation in cells. MicroRNAs are short non-coding RNAs that play an important role in regulation of gene expression. Recently, microRNA-339-5p has been reported to be frequently down-regulated in colorectal cancer, and furthermore, its down-regulation...

متن کامل

MiR-27b directly targets Rab3D to inhibit the malignant phenotype in colorectal cancer

MiRNAs, as oncogenes or as anti-oncogenes, play critically regulated roles in the initiation and progression of colorectal cancer at posttranscriptional level. However, the underlying functions of miR-27b in colorectal cancer remain largely unexplored. Here, we demonstrated miR-27b is significantly down-regulated in colorectal cancer tissues, and decreased miR-27b expression was closely associa...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2016