Qingchao Tang

MicroRNA-25 functions as a potential tumor suppressor in colon cancer by targeting Smad7

Because it is a member of the miR-106b~25 cluster, microRNA-25 (miR-25) is known to be dysregulated in human cancers. However, the expression and role of miR-25 in colon cancer remain unclear. In this study, miR-25 was found to be down-regulated in human colon cancer tissues when compared to those in matched, non-neoplastic mucosa tissues. Functional studies revealed that restoration of miR-25 expression inhibited cell proliferation and migration. In contrast, miR-25 inhibition could promote the proliferation and migratory ability of cells. Stable over-expression of miR-25 also suppressed the growth of colon cancer-cell xenografts in vivo. Furthermore, bioinformatic predictions and experimental validation were used to identify Smad7 as a direct target of miR-25. Functional reverse experiments indicated that the antitumor effects of miR-25 were probably mediated by its repression of Smad7. These results suggest that miR-25 may function as a tumor suppressor by targeting Smad7 in colon cancer. Thus, miR-25 may serve as a potential therapeutic agent or target for cancer therapy.

MicroRNA-93 suppress colorectal cancer development via Wnt/β-catenin pathway downregulating.

MicroRNA-93 (miR-93) is involved in several carcinoma progressions. It has been reported that miR-93 acts as a promoter or suppressor in different tumors. However, till now, the role of miR-93 in colon cancer is unclear. Herein, we have found that expression of miR-93 was lower in human colon cancer tissue and colorectal carcinoma cell lines compared with normal colon mucosa. Forced expression of miR-93 in colon cancer cells inhibits colon cancer invasion, migration, and proliferation. Furthermore, miR-93 may downregulate the Wnt/β-catenin pathway, which was confirmed by measuring the expression level of the β-catenin, axin, c-Myc, and cyclin-D1 in this pathway. Mothers against decapentaplegic homolog 7 (Smad7), as an essential molecular protein for nuclear accumulation of β-catenin in the canonical Wnt signaling pathway, is predicted as a putative target gene of miR-93 by the silico method and demonstrated that it may be suppressed by targeting its 3′UTR. These findings showed that miR-93 suppresses colorectal cancer development via downregulating Wnt/β-catenin, at least in part, by targeting Smad7. This study revealed that miR-93 is an important negative regulator in colon cancer and suggested that miR-93 may serve as a novel therapeutic agent that offers benefits for colon cancer treatment.

Role of MicroRNA 30a Targeting Insulin Receptor Substrate 2 in Colorectal Tumorigenesis

ABSTRACT MicroRNAs (miRNAs) are dysregulated in many types of malignant diseases, including colorectal cancer. miRNA 30a (miR-30a) is a member of the miR-30 family and has been implicated in many types of cancers. In this study, we determined the expression of miR-30a in human colon cancer tissues and cell lines. miR-30a was found to be significantly downregulated in both the tissues and cell lines. Furthermore, overexpression of miR-30a inhibited, while silencing of miR-30a promoted, cell proliferation, migration, and invasion in vitro. Consistently, stable overexpression of miR-30a suppressed the growth of colon cancer cell xenografts in vivo. Moreover, bioinformatic algorithms and luciferase reporter assays revealed that insulin receptor substrate 2 (IRS2) is a direct target of miR-30a. Further functional studies suggested that repression of IRS2 by miR-30a partially mediated the tumor suppressor effect of miR-30a. In addition, miR-30a inhibited constitutive phosphorylation of Akt by targeting IRS2. Additionally, clinicopathological analysis indicated that miR-30a has an inverse correlation with the staging in patients with colon cancer. Taken together, our study provides the first evidence that miR-30a suppressed colon cancer cell growth through inhibition of IRS2. Thus, miR-30a might serve as a promising therapeutic strategy for colon cancer treatment.

Role of microRNA-30c Targeting ADAM19 in Colorectal Cancer

MicroRNAs (miRNAs) are deregulated in a number of cancers including colorectal cancer. MiR-30c belongs to miR-30 family, and is involved in a variety of malignant diseases. In this study, we detected the expression of miR-30c in colon cancer cell lines and clinical colon cancer specimens. MiR-30c was shown to be dramatically down-regulated both in cell lines and cancer tissues. Additionally, miR-30c could inhibit cancer cell growth, migration and invasion in vitro. Consistently, stable over-expression of miR-30c inhibited the growth and lung metastasis of colon cancer cell xenografts in vivo. Furthermore, bioinformatics algorithm and luciferase reporter assay indicated ADAM19 as a direct target of miR-30c. Of interest, further experiments demonstrated that inhibition of ADAM19 by miR-30c partially mediated the anti-tumor effect of miR-30c. Overall, our study provides the new insight that miR-30c inhibited colon cancer cells via targeting ADAM19. Thus, miR-30c might serve as a promising therapeutic strategy for colon cancer treatment.

Colorectal cancer stem cell and chemoresistant colorectal cancer cell phenotypes and increased sensitivity to Notch pathway inhibitor

Colorectal cancer stem cells (Co-CSCs) are a small subpopulation of tumor cells which have been proposed to be tumor-initiating cells in colorectal cancer (CRC) and to be implicated in resistance to standard chemotherapy. Chemoresistance is a common problem in the clinic. However, the interrelation between Co-CSCs and chemoresistant cells has yet to be elucidated. The present study investigated the Co-CSC phenotype in colonospheres and chemoresistant CRC cell lines and aimed to identify targets for therapy. Colonospheres and chemoresistant CRC cells were found to be enriched with the CSC markers CD133 and CD44, and exhibited similar phenotypes. Furthermore, it was found that Notch signaling may simultaneously regulate Co-CSCs and chemoresistant cells and may represent a novel strategy for targeting this pathway in CRC.

Cost Comparison Between Hand-Assisted Laparoscopic Colectomy and Open Colectomy

PURPOSE Our aim was to compare the costs associated with hand-assisted laparoscopic colectomy (HALC) and open colectomy (OC). METHODS The data of patients who underwent either HALC or OC between March 2009 and August 2010 were retrospectively reviewed. The assessed short-term outcomes included operative time, blood lost, retrieved lymph nodes, conversion rates, and complications. Direct costs of operating room, nursing, intensive care, anesthesia, laboratory, pharmacy, radiology, and other costs related to initial hospitalization were compared. RESULTS Forty-two patients underwent HALC, whereas 45 underwent OC. Demographics in both groups were similar. The HALC patients had significantly shorter hospital stays and incision lengths, faster recovery of bowel function, and less blood loss (P<.001). There were no significant differences in operative time (169 minutes for HALC versus 171 minutes for OC), complication rates, or the number of retrieved lymph nodes. Although operative costs were higher for HALC (US

miR-450b-5p Suppresses Stemness and the Development of Chemoresistance by Targeting SOX2 in Colorectal Cancer.

2260 versus

Polymorphic CAG repeat and protein expression of androgen receptor gene in colorectal cancer

1992; P<.001), total costs were not significantly different between both methods (US

Karyopherin alpha 2 expression is a novel diagnostic and prognostic factor for colorectal cancer

5593 vs.

Disparity Expression of Notch1 in Benign and Malignant Colorectal Diseases

5638; P=.29). CONCLUSION Total costs of HALC are not significantly higher compared with OC. HALC is safe and leads to better short-term outcomes than OC.