P52. The role of autophagy in colorectal cancer cells: A pro-survival mechanism

2012 ◽  
Vol 38 (11) ◽  
pp. 1120
Author(s):  
Swethan Alagaratnam ◽  
Ajit Johnson ◽  
Marc Winslet ◽  
Alexander Seifalian ◽  
Barry Fuller ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Survival Mechanism ◽  
Colorectal Cancer Cells

scholarly journals The essential role of TAp73 in bortezomib-induced apoptosis in p53-deficient colorectal cancer cells

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Yasamin Dabiri ◽  
Sara Kalman ◽  
Clara-Marie Gürth ◽  
Jee Young Kim ◽  
Viola Mayer ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Essential Role ◽  
Colorectal Cancer Cells ◽  
Induced Apoptosis

scholarly journals Assessment of TRPV4 Channel and Its Role in Colorectal Cancer Cells

2019 ◽  
Vol 12 (2) ◽  
pp. 629-638
Author(s):  
N. N. Bahari ◽  
S. Y. N. Jamaludin ◽  
A. H. Jahidin ◽  
M. N. Zahary ◽  
A. B. Mohd Hilmi
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Colorectal Cancer ◽  
Expression Levels ◽  
Pharmacological Modulation ◽  
Colorectal Cancer Cells ◽  
Ht 29

The transient receptor potential vanilloid member 4 (TRPV4) is a non-selective calcium (Ca2+)-permeable channel which is widely expressed in different types of tissues including the lungs, liver, kidneys and salivary gland. TRPV4 has been shown to serve as a cellular sensor where it is involved in processes such as osmoregulation, cell volume regulation and thermoregulation. Emerging evidence suggests that TRPV4 also plays important roles in several aspects of cancer progression. Despite the reported roles of TRPV4 in several forms of cancers, the role of TRPV4 in human colorectal cancer remains largely unexplored. In the present study, we sought to establish the potential role of TRPV4 in colorectal cancer by assessing TRPV4 expression levels and investigating whether TRPV4 pharmacological modulation may alter cell proliferation, cell cycle and cell death in colorectal cancer cells. Quantitative real-time PCR analysis revealed that TRPV4 mRNA levels were significantly lower in HT-29 cells than normal colon CCD-18Co cells. However, TRPV4 mRNA was absent in HCT-116 cells. Pharmacological activation of TRPV4 with GSK1016790A significantly enhanced the proliferation of HT-29 cells while TRPV4 inhibition using RN 1734 decreased their proliferation. Increased proliferation in GSK1016790A-treated HT-29 cells was attenuated by co-treatment with RN 1734. Pharmacological modulation of TRPV4 had no effect on the cell cycle progression but promoted cell death in HT-29 cells. Taken together, these findings suggest differential TRPV4 expression levels in human colorectal cancer cells and that pharmacological modulation of TRPV4 produces distinct effects on the proliferation and induces cell death in HT-29 cells.

scholarly journals Nei Endonuclease VIII-Like1 (NEIL1) Inhibits Apoptosis of Human Colorectal Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Wanjuan Xue ◽  
Yongcheng Liu ◽  
Ningning Xin ◽  
Jiyu Miao ◽  
Juan Du ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Human Colon ◽  
Caspase 9 ◽  
Human Colon Cancer ◽  
Expression Levels ◽  
Colorectal Cancer Cells ◽  
Human Colorectal Cancer Cells

The study is aimed at investigating the role of Nei endonuclease VIII-like1 (NEIL1) in the pathogenesis of colorectal cancer (CRC). The human CRC (HCT116 and SW480) cells were subjected to the siRNA silencing and recombinant plasmid overexpression of NEIL1. Transfection of siNEIL1 significantly inhibited the cell growth. It also increased the Bax expression levels, while it decreased the Bcl-2 expression levels in human CRC cells, leading the Bax/Bcl-2 balance toward apoptosis. Moreover, the apoptosis was promoted through the caspase-9 signaling pathway. One the other hand, high expression of NEIL1 promoted the cell viability and reduced the apoptosis, inducing the balance of Bax/Bcl-2 in the human colon cancer cells to be antiapoptotic. In addition, the caspase-9 signaling pathway inhibited apoptosis, contrary to the results obtained by downregulating NEIL1 expression. Furthermore, NEIL1 was negatively regulated by miR-7-5p, indicating that miR-7-5p inhibited the NEIL1 expression after transcription. Overexpression of miR-7-5p reversed the effects of NEIL1 on these CRC cells. In conclusion, NEIL1 promotes the proliferation of CRC cells, which is regulated negatively by miR-7-5p. These findings suggest that NEIL1 is a potential therapeutic target for CRC.

The role of spermidine/spermine N1-acetyltransferase in determining response to chemotherapeutic agents in colorectal cancer cells

2007 ◽  
Vol 6 (1) ◽  
pp. 128-137 ◽  
Author(s):  
Wendy L. Allen ◽  
Estelle G. McLean ◽  
John Boyer ◽  
Andrea McCulla ◽  
Peter M. Wilson ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Chemotherapeutic Agents ◽  
Colorectal Cancer Cells

scholarly journals A novel cell type-specific role of p38α in the control of autophagy and cell death in colorectal cancer cells

2006 ◽  
Vol 14 (4) ◽  
pp. 693-702 ◽  
Author(s):  
F Comes ◽  
A Matrone ◽  
P Lastella ◽  
B Nico ◽  
F C Susca ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Specific Role ◽  
Cell Type ◽  
Colorectal Cancer Cells ◽  
Cell Type Specific

scholarly journals Role of MCP-1 in alcohol-induced aggressiveness of colorectal cancer cells

2015 ◽  
Vol 55 (5) ◽  
pp. 1002-1011 ◽  
Author(s):  
Mei Xu ◽  
Siying Wang ◽  
Yuanlin Qi ◽  
Li Chen ◽  
Jacqueline A. Frank ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Colorectal Cancer Cells

scholarly journals Context-specific role of SOX9 in NF-Y mediated gene regulation in colorectal cancer cells

2015 ◽  
Vol 43 (13) ◽  
pp. 6257-6269 ◽  
Author(s):  
Zhongcheng Shi ◽  
Chi-I Chiang ◽  
Paul Labhart ◽  
Yanling Zhao ◽  
Jianhua Yang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gene Regulation ◽  
Cancer Cells ◽  
Specific Role ◽  
Colorectal Cancer Cells ◽  
Context Specific

Effect of neuropilin-2 expression on TGF-β1-epithelial-mesenchymal transition in colorectal cancer cells.

2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 414-414
Author(s):  
C. Grandclement ◽  
R. Bedel ◽  
B. Kantelip ◽  
E. Viel ◽  
J. Remy Martin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Human Colon ◽  
Mesenchymal Transition ◽  
Colorectal Cancer Cells ◽  
Tgf Β1

414 Background: Initially characterized as neuronal receptors, Neuropilins (NRPs) were also found to be expressed in endothelial cells and subsequently were shown to play a role in the development of the vascular system. NRP family consists of two genes, neuropilin-1 (NRP1) and neuropilin-2 (NRP2).The multiple functions of NRPs were recently highlighted by the identification of NRP role in oncogenesis. In this study, we first confirmed the role of NRP2 in tumor progression. We also extended the understanding of NRP2 oncogenic functions by investigating the ability of NRP2 to orchestrate epithelial-mesenchymal transition (EMT) in colorectal cancer cells. Methods: We have generated human colon cancer cell lines transfected with NRP2 transgene or siRNA to investigate NRP2 involvement in EMT. First, the oncogenic functions of NRP2 were studied in vitro by MTT, soft agar, invasion assays and in vivo using xenografts experiments. Ability of NRP2 to orchestrate EMT was then investigated by flow cytometry, immunohistochemical (IHC) staining, western-blotting and quantitative real-time PCR. Results: IHC staining revealed that NRP2 is expressed in human colon and breast carcinomas while it is not expressed in healthy tissues. Then, we confirmed that NRP2 increases tumor proliferation, colony formation, invasion and xenograft formation. Moreover, NRP2-expressing cells displayed an immunohistochemical phenotype of EMT characterized by the loss of E-Cadherin and an increase of vimentin. Furthermore, NRP2 expression promotes transforming-growth factor-β1 (TGF- β1) signaling, leading to an increased phosphorylation of the Smad2/3 complex in colorectal cancer cell lines. Specific inhibition of NRP2 using siRNA or treatment with specific TGFβRI kinase inhibitors prevented this phosphorylation and the EMT, suggesting that NRP2 cooperates with TGFRI to promote EMT in colorectal carcinoma. Conclusions: Our findings have reinforced the essential role of NRP2 in cancer progression and demonstrated that NRP2 expression confers to tumor cell lines the hallmarks of EMT. Moreover, in the current work, we present evidence for the therapeutic value of NRP2 targeting. No significant financial relationships to disclose.

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