MicroRNA-130a is upregulated in colorectal cancer and promotes cell growth and motility by directly targeting forkhead box F2
نویسندگان
چکیده
Colorectal cancer (CRC) is one of the most prevalent cancers among males and females worldwide. Despite progress in diagnostic and therapeutic strategies for CRC patients, the prognosis for patients with advanced CRC remains poor. MicroRNAs (miRNAs/miRs) are a class of highly conserved short, endogenously expressed and single‑stranded non‑coding RNAs. In recent years, increasing studies have demonstrated that dysregulation of miRNAs is closely associated with CRC carcinogenesis and progression. The aim of the present study was to explore the expression, roles and underlying molecular mechanism of miR‑130a in CRC. The results indicated that miR‑130a was significantly upregulated in CRC, and that miR‑130a expression levels were correlated with TNM stage and lymph node metastasis of CRC. Inhibition of miR‑130a markedly suppressed colorectal cancer cell proliferation, migration and invasion. Furthermore, forkhead box F2 (FOXF2) was identified as a direct downstream target gene of miR‑130a in colorectal cancer. Downregulation of FOXF2 could partially reverse the functions induced by miR‑130a under‑expression in CRC cells. These findings suggested that miR‑130a can regulate FOXF2 and function as an oncogene in CRC. Therefore, miR‑130a may serve as a useful therapeutic agent for miRNA‑based CRC targeted therapy.
منابع مشابه
MicroRNA-544 promotes colorectal cancer progression by targeting forkhead box O1
Dysregulation of microRNAs has been confirmed to serve an important role in cancer development and progression. However, the role of microRNA (miR)-544 in colorectal cancer progression remains unknown. In the present study, it was observed that the expression level of miR-544 was increased in breast cancer cell lines and tissues using the quantitative polymerase chain reaction. Overexpression o...
متن کاملMicroRNA-182 promotes proliferation and metastasis by targeting FOXF2 in triple-negative breast cancer
Triple-negative breast cancer (TNBC), the most aggressive subtype of breast cancer (BC), is characterized as high proliferation, young age and poor prognosis. MicroRNA-182 (miR-182) was reported to have oncogenic potential in many cancers. We aimed to elucidate pathobiological effects of miR-182 expression by targeting forkhead-box F2 (FOXF2) in TNBC. In this study, we explored the functional r...
متن کاملmiR-182 promotes cell growth and invasion by targeting forkhead box F2 transcription factor in colorectal cancer.
Forkhead box F2 transcription factor (FoxF2) has been described to promote organ development, extracellular matrix (ECM) synthesis and epithelial-mesenchymal interaction. Although recent studies reported decreased FoxF2 expression in several types of cancers, indicating its potential role in carcinogenesis, the mechanistic role of FoxF2 is yet to be explored. MicroRNAs (miRNAs) are strongly imp...
متن کاملThe Oncogenic Role of microRNA-130a/301a/454 in Human Colorectal Cancer via Targeting Smad4 Expression
Transforming growth factor (TGF)-β/Smad signaling plays an important role in colon cancer development, progression and metastasis. In this study we demonstrated that the microRNA-130a/301a/454 family is up-regulated in colon cancer tissues compared to paired adjacent normal mucosa, which share the same 3'-untranslational region (3'-UTR) binding seed sequence and are predicated to target Smad4. ...
متن کاملMicroRNA-130a inhibits cell proliferation, invasion and migration in human breast cancer by targeting the RAB5A.
MiR-130a has been demonstrated to play important roles in many types of cancers. Nevertheless, its biological function in breast cancer remains largely unknown. In this study, we found that the expression level of miR-130a was down-regulated in breast cancer tissues and cells. Overexpression of miR-130a was able to inhibit cell proliferation, invasion and migration in MCF7 and MDA-MB-435 cells....
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 16 شماره
صفحات -
تاریخ انتشار 2017