scholarly journals miR-29b suppresses tumor growth and metastasis in colorectal cancer via downregulating Tiam1 expression and inhibiting epithelial–mesenchymal transition

2014 ◽  
Vol 5 (7) ◽  
pp. e1335-e1335 ◽  
Author(s):  
B Wang ◽  
W Li ◽  
H Liu ◽  
L Yang ◽  
Q Liao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tumor Growth And Metastasis

scholarly journals Integrin α9β1 promotes malignant tumor growth and metastasis by potentiating epithelial-mesenchymal transition

Oncogene ◽  
2012 ◽  
Vol 32 (2) ◽  
pp. 141-150 ◽  
Author(s):  
S K Gupta ◽  
S Oommen ◽  
M-C Aubry ◽  
B P Williams ◽  
N E Vlahakis
Keyword(s):  
Tumor Growth ◽  
Malignant Tumor ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tumor Growth And Metastasis

scholarly journals Nicotinic Acetylcholine Receptor Signaling in Tumor Growth and Metastasis

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Sandeep Singh ◽  
Smitha Pillai ◽  
Srikumar Chellappan
Keyword(s):  
Tumor Growth ◽  
Nicotinic Acetylcholine Receptors ◽  
Tobacco Smoke ◽  
Acetylcholine Receptors ◽  
Epithelial Mesenchymal Transition ◽  
Antitumor Effects ◽  
Nicotinic Acetylcholine ◽  
Mesenchymal Transition ◽  
Promote Cell Proliferation ◽  
Tumor Growth And Metastasis

Cigarette smoking is highly correlated with the onset of a variety of human cancers, and continued smoking is known to abrogate the beneficial effects of cancer therapy. While tobacco smoke contains hundreds of molecules that are known carcinogens, nicotine, the main addictive component of tobacco smoke, is not carcinogenic. At the same time, nicotine has been shown to promote cell proliferation, angiogenesis, and epithelial-mesenchymal transition, leading to enhanced tumor growth and metastasis. These effects of nicotine are mediated through the nicotinic acetylcholine receptors that are expressed on a variety of neuronal and nonneuronal cells. Specific signal transduction cascades that emanate from different nAChR subunits or subunit combinations facilitate the proliferative and prosurvival functions of nicotine. Nicotinic acetylcholine receptors appear to stimulate many downstream signaling cascades induced by growth factors and mitogens. It has been suggested that antagonists of nAChR signaling might have antitumor effects and might open new avenues for combating tobacco-related cancer. This paper examines the historical data connecting nicotine tumor progression and the recent efforts to target the nicotinic acetylcholine receptors to combat cancer.

scholarly journals PAICS, a Purine Nucleotide Metabolic Enzyme, is Involved in Tumor Growth and the Metastasis of Colorectal Cancer

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 772 ◽  
Author(s):  
Sumit Agarwal ◽  
Balabhadrapatruni V. S. K. Chakravarthi ◽  
Michael Behring ◽  
Hyung-Gyoon Kim ◽  
Darshan S. Chandrashekar ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
De Novo ◽  
Epithelial Mesenchymal Transition ◽  
Positron Emission Tomography Imaging ◽  
Metabolic Enzyme ◽  
Mesenchymal Transition ◽  
Improve Patient Survival ◽  
Positron Emission ◽  
Cell Dissemination

The identification of colorectal cancer (CRC) molecular targets is needed for the development of drugs that improve patient survival. We investigated the functional role of phosphoribosylaminoimidazole carboxylase, phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS), a de novo purine biosynthetic enzyme involved in DNA synthesis, in CRC progression and metastasis by using cell and animal models. Its clinical utility was assessed in human CRC samples. The expression of PAICS was regulated by miR-128 and transcriptionally activated by Myc in CRC cells. Increased expression of PAICS was involved in proliferation, migration, growth, and invasion of CRC cells irrespective of the p53 and microsatellite status. In mice, the depletion of PAICS in CRC cells led to reduced tumor growth and metastatic cell dissemination to the liver, lungs, and bone. Positron emission tomography imaging showed significantly reduced metastatic lesions in stable PAICS knockdown CRC cells. In cells with PAICS knockdown, there was upregulation of the epithelial mesenchymal transition marker, E-cadherin, and bromodomain inhibitor, JQ1, can target its increased expression by blocking Myc. PAICS was overexpressed in 70% of CRCs, and was associated with poor 5-year survival independent of the pathologic stage, patient’s race, gender, and age. Overall, the findings point to the usefulness of PAICS targeting in the treatment of aggressive colorectal cancer.

Activation of AKT signaling promotes epithelial-mesenchymal transition and tumor growth in colorectal cancer cells

2013 ◽  
Vol 53 (S1) ◽  
pp. E151-E160 ◽  
Author(s):  
Suman Suman ◽  
Vittal Kurisetty ◽  
Trinath P. Das ◽  
Aditi Vadodkar ◽  
Gabriel Ramos ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Mesenchymal Transition ◽  
Colorectal Cancer Cells

scholarly journals MicroRNA-150 suppresses epithelial-mesenchymal transition, invasion, and metastasis in prostate cancer through the TRPM4-mediated β-catenin signaling pathway

2019 ◽  
Vol 316 (4) ◽  
pp. C463-C480 ◽  
Author(s):  
Xi Hong ◽  
Jian-Jun Yu
Keyword(s):  
Prostate Cancer ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Transient Receptor Potential ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Transient Receptor Potential Melastatin ◽  
Tumor Growth And Metastasis

Prostate cancer (PCa) remains one of the leading causes of cancer-related deaths among males. The aim of the current study was to investigate the ability of microRNA-150 (miR-150) targeting transient receptor potential melastatin 4 (TRPM4) to mediate epithelial-mesenchymal transition (EMT), invasion, and metastasis through the β-catenin signaling pathway in PCa. Microarray analysis was performed to identify PCa-related differentially expressed genes, after which both the mirDIP and TargetScan databases were employed in the prediction of the miRNAs regulating TRPM4. Immunohistochemistry and RT-qPCR were conducted to determine the expression pattern of miR-150 and TRPM4 in PCa. The relationship between miR-150 and TRPM4 expression was identified. By perturbing miR-150 and TRPM4 expression in PCa cells, cell proliferation, migration, invasion, cycle, and apoptosis as well as EMT markers were determined accordingly. Finally, tumor growth and metastasis were evaluated among nude mice. Higher TRPM4 expression and lower miR-150 expression and activation of the β-catenin signaling pathway as well as EMT stimulation were detected in the PCa tissues. Our results confirmed TRPM4 as a target of miR-150. Upregulation of miR-150 resulted in inactivation of the β-catenin signaling pathway. Furthermore, the upregulation of miR-150 or knockdown of TRPM4 was observed to suppress EMT, proliferation, migration, and invasion in vitro in addition to restrained tumor growth and metastasis in vivo. The evidence provided by our study highlights the involvement of miR-150 in the translational suppression of TRPM4 and the blockade of the β-catenin signaling pathway, resulting in the inhibition of PCa progression.

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