MiR-34b inhibits the proliferation and promotes apoptosis in colon cancer cells by targeting Wnt/β-catenin signaling pathway

Abstract Colon cancer is one of the leading cause of cancer deaths that is severely threatening human health. Several microRNAs (miRNAs) have been found to be associated with the tumor genesis of colon cancer. The present study determined the expression of miR-34b in patients with colon cancer and studied the molecular mechanism of miR-34b in the proliferation and apoptosis of human colon cancer Caco-2 cells in vitro. In colon cancer patients, the expression of miR-34b was decreased in tumor tissues when compared with the adjacent non-tumor tissues. Furthermore, overexpression of miR-34b inhibited proliferation, migration and invasion, while promoted apoptosis in colon cancer cells. The online bioinformatics sites predicted possible regulatory genes of miR-34b and luciferase reporter assay verify that β-catenin was a direct target of miR-34b. Furthermore, miR-34b overexpression significantly decreased the expression of genes associated with Wnt/β-catenin signaling pathway. In conclusion, our results suggest that miR-34b may inhibit migration and invasion of human colon cancer cells by regulating Wnt/β-catenin signaling and miR-34b may be a key target for the treatment and diagnosis of colon cancer.

Download Full-text

Validation of TPX2 as a novel prognostic marker for malignant progression and metastasis of colon cancer.

Journal of Clinical Oncology ◽

10.1200/jco.2013.31.4_suppl.442 ◽

2013 ◽

Vol 31 (4_suppl) ◽

pp. 442-442 ◽

Cited By ~ 1

Author(s):

Ping Wei ◽

Dawei Li ◽

Ye Xu ◽

Sanjun Cai

Keyword(s):

Colon Cancer ◽

Cancer Cells ◽

Human Colon ◽

Clinical Staging ◽

Migration And Invasion ◽

Colon Cancer Cells ◽

Human Colon Cancer ◽

A Genome

442 Background: We previously identified aberrant overexpression of TPX2 in colon cancer by using a genome-wide gene expression profiling analysis. Here, we aimed to investigate its expression pattern, clinical significance, and biological function in colon cancer. Methods: The expression of TPX2 was analyzed in human colon cancer cell lines and tumor samples. The effect of TPX2 on cell proliferation, tumorigenesis and metastasis was examined in vitro and in vivo. Results: Overexpression of TPX2 was found in metastatic lesion of colon cancer, significantly higher than primary cancererous tissue and normal colon mucosa. Overexpression of TPX2 was significantly associated with the clinical staging, vessel invasion and metastasis. In survival analyses, patients with TPX2 expression had worse overall survival and metastasis free survival, suggesting that deregulation of TPX2 may contribute to the metastasis of colon cancer. Consistently, Silencing TPX2 inhibited proliferation and tumorigenicity of colon cancer cells both in vitro and in vivo. Strikingly, we found that TPX2 knockdown significantly attenuated the migration and invasion ability of colon cancer cells, which was further shown to be mechanistically associated with AKT mediated MMP9 activity. Conclusions: These findings suggest that TPX2 plays an important role in promoting tumorigenesis and metastasis of human colon cancer and may represent a novel prognostic biomarker and therapeutic target for the disease.

Download Full-text