scholarly journals siPRDX2-elevated DNM3 inhibits the proliferation and metastasis of colon cancer cells via AKT signaling pathway

2019 ◽  
Vol Volume 11 ◽  
pp. 5799-5811 ◽  
Author(s):  
Yini Ma ◽  
Liying Guan ◽  
Yanxin Han ◽  
Yi Zhou ◽  
Xiaoming Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Colon Cancer Cells ◽  
Akt Signaling Pathway ◽  
Proliferation And Metastasis

scholarly journals Angiomotin promotes the malignant potential of colon cancer cells by activating the YAP-ERK/PI3K-AKT signaling pathway

2016 ◽  
Vol 36 (6) ◽  
pp. 3619-3626 ◽  
Author(s):  
Yan Zhang ◽  
Jun Yuan ◽  
Xinli Zhang ◽  
Futang Yan ◽  
Minggang Huang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Malignant Potential ◽  
Colon Cancer Cells ◽  
Akt Signaling Pathway

scholarly journals Knockdown of PRDX2 sensitizes colon cancer cells to 5-FU by suppressing the PI3K/AKT signaling pathway

2017 ◽  
Vol 37 (3) ◽  
Author(s):  
Jun Xu ◽  
Shouru Zhang ◽  
Rong Wang ◽  
Xingye Wu ◽  
Li Zeng ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Cancer Resistance ◽  
Colon Cancer Cells ◽  
Akt Signaling Pathway ◽  
Ros Scavenging ◽  
Bax Protein

Although, 5-Fluorouracil (5-FU) remains widely used in adjuvant therapy in patients with colon cancer, resistance to 5-FU-based chemotherapy is an important reason for treatment failure. Recent studies have reported that an enhanced reactive oxygen species (ROS) scavenging system shows drug resistance to 5-FU. Peroxiredoxin-2 (PRDX2), is an important member of the ROS scavenging system, and may be a potential target that promotes chemosensitivity to 5-FU in colon cancer. Here, we depleted PRDX2 by PRDX2-shRNA-LV transduction in two colon cancer cell lines and found that in vitro PRDX2 knockdown facilitates cell death, and apoptosis in 5-FU-treated colon cancer cells. In addition, we found that PRDX2 depletion in mice treated with 5-FU resulted in, inhibition of tumor growth, compared with mice treated with 5-FU alone. Our data also suggested that the PI3K/AKT signaling pathway links PRDX2 with 5-FU-induced apoptosis in colon cancer. Furthermore, when PRDX2 was overexpressed in colon cancer cells, we found increased p-AKT protein expression and reduced Bcl-2/Bax protein expression. PRDX2 and p-AKT protein expression were analyzed by immunohistochemistry technology in human colon carcinoma tissues. Pearson correlation coefficient is 0.873 and P<0.05. PRDX2 depletion led to reduced p-AKT expression and PI3K/AKT pathway inhibition promoted cell apoptosis in HT29 cell line. Taken together, our study suggests that decreasing the expression of PRDX2 could be a promising strategy for increasing the sensitivity of colon cancer cells to 5-FU.

scholarly journals MACC1 facilitates chemoresistance and cancer stem cell-like properties of colon cancer cells through the PI3K/AKT signaling pathway

2017 ◽  
Vol 16 (6) ◽  
pp. 8747-8754 ◽  
Author(s):  
Jiankai Wang ◽  
Wenjuan Wang ◽  
Hongyi Cai ◽  
Binbin Du ◽  
Lijuan Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Colon Cancer Cells ◽  
Akt Signaling Pathway

scholarly journals Fibroblast-derived CXCL12 regulates PTEN expression and is associated with the proliferation and invasion of colon cancer cells via PI3k/Akt signaling

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Jiachi Ma ◽  
Xiaowen Sun ◽  
Yimin Wang ◽  
Bangling Chen ◽  
Liyu Qian ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Stromal Cells ◽  
Metastatic Potential ◽  
Underlying Mechanism ◽  
Akt Signaling ◽  
Colon Cancer Cells ◽  
Proliferation And Invasion

Abstract Background Stromal-derived CXCL12 play an important role which influence the proliferation and invasiveness of colon cancer in microenvironment. The present study aimed to analyze the underlying mechanism by which CXCL12 and tumour suppressor protein phosphatase and tensin homologue deleted on chromosome 10 (PTEN) influences the metastatic potential of colon cancer and internal relation of colon cancer and stromal cells. Methods RT-PCR and western blot were detected the expression of CXCL12, CXCR4 and PTEN in colon cancer cells and stromal cells. The co-operative effects of CXCL12 and PTEN on proliferation and invasion of colon cancer cells were evaluated by real-time PCR, proliferation and invasion assays using an in vitro system consisting of co-cultured cancer cells and stromal cells. We eventually investigated activation of PI3K/Akt signaling by CXCL12 regulate PTEN and involved in the metastatic process of colon cancer. In addition, we also examine how the knockdown of PTEN influences proliferation and invasion and correlate with CXCL12/CXCR4/PI3K/Akt, determination of PTEN up-down-stream targets that preferentially contribute to tumorigenesis. Results Blockage of PTEN phosphorylation led to a stronger enhancement of cell proliferation and invasion upon stimulation with CXCL12 via its activation of the PI3K/Akt signaling pathway. Furthermore, knockdown of PTEN by siRNA transfection was also found to enhance the activation of the PI3K/Akt pathway, thereby promoting cell invasion and proliferation. CXCL12 induced transcriptional down-regulation of activated PTEN and this signaling pathway promotes cell survival. CXCL12/CXCR4/PI3K/Akt cascade may be critical for colon cancer cells to metastasize. Conclusions Based on our results, we suggest that the modification of CXCR4, PTEN, or PI3K function might be promising new therapeutic approaches to inhibit the aggressive spread of colon cancer.

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