scholarly journals TLE4 promotes colorectal cancer progression through activation of JNK/c-Jun signaling pathway

Oncotarget ◽  
2015 ◽  
Vol 7 (3) ◽  
pp. 2878-2888 ◽  
Author(s):  
Shu-Yang Wang ◽  
Ke Gao ◽  
Dan-Ling Deng ◽  
Juan-Juan Cai ◽  
Zhi-Yuan Xiao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Colorectal Cancer Progression

Lactobacillus species inhibitory effect on colorectal cancer progression through modulating the Wnt/β-catenin signaling pathway

2020 ◽  
Vol 470 (1-2) ◽  
pp. 1-13
Author(s):  
Roya Ghanavati ◽  
Abolfazl Akbari ◽  
Fahime Mohammadi ◽  
Parisa Asadollahi ◽  
Abdolreza Javadi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Inhibitory Effect ◽  
Lactobacillus Species ◽  
Colorectal Cancer Progression

scholarly journals Upregulation of OSBPL3 by HIF1A promotes colorectal cancer progression through activation of RAS signaling pathway

2020 ◽  
Vol 11 (7) ◽  
Author(s):  
Hong-li Jiao ◽  
Bin-shu Weng ◽  
Shan-shan Yan ◽  
Zi-mo Lin ◽  
Shu-yang Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Ras Signaling ◽  
Invasion And Metastasis ◽  
In Vivo Models ◽  
Ras Signaling Pathway ◽  
Colorectal Cancer Progression

AbstractOxysterol-binding protein like protein 3 (OSBPL3) has been shown involving in the development of several human cancers. However, the relationship between OSBPL3 and colorectal cancer (CRC), particularly the role of OSBPL3 in the proliferation, invasion and metastasis of CRC remains unclear. In this study, we investigated the role of OSBPL3 in CRC and found that its expression was significantly higher in CRC tissues than that in normal tissues. In addition, high expression of OSBPL3 was closely related to poor differentiation, advanced TNM stage and poor prognosis of CRC. Further experiments showed that over-expression of OSBPL3 promoted the proliferation, invasion and metastasis of CRC in vitro and in vivo models. Moreover, we revealed that OSBPL3 promoted CRC progression through activation of RAS signaling pathway. Furthermore, we demonstrated that hypoxia induced factor 1 (HIF-1A) can regulate the expression of OSBPL3 via binding to the hypoxia response element (HRE) in the promoter of OSBPL3. In summary, Upregulation of OSBPL3 by HIF1A promotes colorectal cancer progression through activation of RAS signaling pathway. This novel mechanism provides a comprehensive understanding of both OSBPL3 and the RAS signaling pathway in the progression of CRC and indicates that the HIF1A–OSBPL3–RAS axis is a potential target for early therapeutic intervention in CRC progression.

Upregulation lnc-NEAT1 contributes to colorectal cancer progression through sponging miR-486-5p and activating NR4A1/Wnt/β-catenin pathway

2020 ◽  
pp. 1-11
Author(s):  
Zhining Liu ◽  
Yimei Gu ◽  
Xiaohu Cheng ◽  
Heng Jiang ◽  
Yang Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Colorectal Cancer Cells ◽  
Colorectal Cancer Progression ◽  
Colorectal Cancer Patients ◽  
Cancer Tissues

Colorectal cancer is a major public health problem and fourth guiding cause of cancer-induced mortality worldwide. The five-year survival rate for patients with colorectal cancer remains poor, and almost half of colorectal cancer patients present recurrence and die within five years. The increasing studies showed that long non-coding RNA (lncRNA) was involved in colorectal cancer. Therefore, this study was used to explore molecular mechanisms of nuclear paraspeckle assembly transcript 1 (NEAT1) in colorectal cancer. The real-time quantitative polymerase chain reaction (RT-qPCR) was employed to estimate the expression levels of NEAT1, Nuclear receptor 4 A1 (NR4A1), and miR-486-5p in colorectal cancer tissues and cells. Kaplan-Meier curve was conducted to analyze relationship between survival time of colorectal cancer patients and level of NEAT1. The protein levels of NR4A1, β-catenin, c-Myc, and cyclinD1 were assessed with western blot assay. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and flow cytometry assays were performed to evaluate proliferation and apoptosis of colorectal cancer cells, respectively. The migration and invasion abilities of cells were examined by transwell assay. The relationship between miR-486-5p and NEAT1 or NR4A1 was confirmed by dual-luciferase reporter assay. We found NEAT1 and NR4A1 were highly expressed in colorectal cancer tissues and cell lines compared with controls. Loss-functional experiments revealed that knockdown of NEAT1 or NR4A1 repressed proliferation and motility, while inducing apoptosis of colorectal cancer cells. The gain of NR4A1 could abolish NEAT1 silencing-induced effects in colorectal cancer cells. In addition, NEAT1 contributed to colorectal cancer progression through mediating NR4A1/Wnt/β-catenin signaling pathway. In conclusion, NEAT1 stimulated colorectal cancer progression via acting as competing endogenous RNA to sponge miR-486-5p and regulate NR4A1/Wnt/β-catenin signaling pathway.

scholarly journals ALKAL1 gene silencing prevents colorectal cancer progression via suppressing Sonic Hedgehog (SHH) signaling pathway

2021 ◽  
Vol 12 (1) ◽  
pp. 150-162
Author(s):  
Shasha Chen ◽  
Bin Wang ◽  
Xuekun Fu ◽  
Yanfang Liang ◽  
Xingxing Chai ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gene Silencing ◽  
Signaling Pathway ◽  
Sonic Hedgehog ◽  
Cancer Progression ◽  
Shh Signaling ◽  
Colorectal Cancer Progression

scholarly journals TMEM100 Modulates TGF-β Signaling Pathway to Inhibit Colorectal Cancer Progression

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Huixia Li ◽  
Chuan Cheng ◽  
Weibo You ◽  
Jiujian Zheng ◽  
Jie Xu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Transmembrane Protein ◽  
Expression Data ◽  
Mrna Expression Data ◽  
Colorectal Cancer Progression ◽  
Inhibitor Gene

Objectives. This study investigated the functional mechanism of transmembrane protein 100 (TMEM100) as a tumor inhibitor gene in CRC cells and offered a reference for the treatment of CRC. Methods. The mRNA expression data of CRC were acquired from the TCGA database to mine differentially expressed mRNAs. The role of TMEM100 in the progression of CRC cells was evaluated by MTT, colony formation, scratch healing, and Transwell assays. The influence of TMEM100 on the TGF-β signaling pathway was detected by western blot. Results. TMEM100 was markedly lowly expressed in CRC. CRC cell growth was significantly suppressed by overexpressing TMEM100 but noticeably facilitated by silencing TMEM100. Overexpression of TMEM100 inhibited the activation of the TGF-β signaling pathway, thus inhibiting malignant progression of CRC. Conclusion. TMEM100 is lowly expressed in CRC, which can suppress CRC cell growth by regulating the TGF-β signaling pathway.

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