Azaindolylsulfonamides, with a More Selective Inhibitory Effect on Histone Deacetylase 6 Activity, Exhibit Antitumor Activity in Colorectal Cancer HCT116 Cells

2014 ◽  
Vol 57 (10) ◽  
pp. 4009-4022 ◽  
Author(s):  
Hsueh-Yun Lee ◽  
An-Chi Tsai ◽  
Mei-Chuan Chen ◽  
Po-Jung Shen ◽  
Yun-Ching Cheng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Antitumor Activity ◽  
Histone Deacetylase ◽  
Inhibitory Effect ◽  
Histone Deacetylase 6 ◽  
Hct116 Cells

Pyrimidinedione-mediated selective histone deacetylase 6 inhibitors with antitumor activity in colorectal cancer HCT116 cells

2015 ◽  
Vol 13 (40) ◽  
pp. 10226-10235 ◽  
Author(s):  
Yi-Min Liu ◽  
Hsueh-Yun Lee ◽  
Mei-Jung Lai ◽  
Shiow-Lin Pan ◽  
Hsiang-Ling Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Antitumor Activity ◽  
Histone Deacetylase ◽  
Histone Deacetylase 6 ◽  
Hct116 Cells

We synthesized a series of pyrimidinedione derivatives and evaluated their activities.

Discovery of a New Isoxazole-3-hydroxamate-Based Histone Deacetylase 6 Inhibitor SS-208 with Antitumor Activity in Syngeneic Melanoma Mouse Models

2019 ◽  
Vol 62 (18) ◽  
pp. 8557-8577 ◽  
Author(s):  
Sida Shen ◽  
Melissa Hadley ◽  
Kseniya Ustinova ◽  
Jiri Pavlicek ◽  
Tessa Knox ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Histone Deacetylase ◽  
Mouse Models ◽  
Histone Deacetylase 6

scholarly journals Aspirin suppresses chemoresistance and enhances antitumor activity of 5-Fu in 5-Fu-resistant colorectal cancer by abolishing 5-Fu-induced NF-κB activation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jinbo Fu ◽  
Yiming Xu ◽  
Yushan Yang ◽  
Yun Liu ◽  
Lulu Ma ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Antitumor Activity ◽  
Therapeutic Agent ◽  
Inhibitory Effect ◽  
Antitumor Activities ◽  
Tumor Cell Apoptosis ◽  
Tumor Growth And Metastasis ◽  
Resistant Cells

AbstractChemoresistance to 5-fluorouracil (5-Fu)-based chemotherapy is a leading obstacle in achieving effective treatment for colorectal cancer (CRC). Typically, NF-κB activation induced by the chemotherapeutics themselves is an important cause resulting in chemoresistance. Specifically, NF-κB activation can inhibit tumor cell apoptosis and induce chemoresistance. Drugs that can prevent NF-κB activation induced by chemotherapeutics are urgently needed to overcome chemoresistance. Obviously, aspirin is one of these agents, which has been demonstrated to possess antitumor activities and as an inhibitor of NF-κB. The current study aimed to investigate whether aspirin was able to overcome the chemoresistance to 5-Fu in CRC, together with the potential synergistic mechanisms. Our results suggested that aspirin remarkably potentiated the inhibitory effect of 5-Fu on the growth and invasion of resistant cells in vitro. In vivo, aspirin markedly enhanced the antitumor activity of 5-Fu in suppressing tumor growth and metastasis, and down-regulating the expression of NF-κB-regulated genes in the 5-Fu-resistant cells. Obviously, aspirin completely eradicated the 5-Fu-induced NF-κB activation, without inducing pronounced adverse effects. Taken together, findings in this study suggest that aspirin can reverse chemoresistance and potentiate the antitumor effect of 5-Fu, which is achieved through abolishing the 5-Fu-induced NF-κB activation, suggesting that aspirin may be a promising adjuvant therapeutic agent for CRC.

scholarly journals The lncRNA FEZF1-AS1 Promotes the Progression of Colorectal Cancer Through Regulating OTX1 and Targeting miR-30a-5p

2020 ◽  
Vol 28 (1) ◽  
pp. 51-63 ◽  
Author(s):  
Jing Li ◽  
Lian-mei Zhao ◽  
Cong Zhang ◽  
Meng Li ◽  
Bo Gao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Mesenchymal Transition ◽  
Reporter Assays ◽  
Direct Target ◽  
Next Generation Sequencing Ngs ◽  
Hct116 Cells

Long noncoding RNAs (lncRNAs) participate in and regulate the biological process of colorectal cancer (CRC) progression. Our previous research identified differentially expressed lncRNAs in 10 CRC tissues and 10 matched nontumor tissues by next-generation sequencing (NGS). In this study, we identified an lncRNA, FEZF1 antisense RNA 1 (FEZF1-AS1), and further explored its function and mechanism in CRC. We verified that FEZF1-AS1 is highly expressed in CRC tissues and cell lines. Through functional experiments, we found that reduced levels of FEZF1-AS1 significantly suppressed CRC cell migration, invasion, and proliferation and inhibited tumor growth in vivo. Mechanistically, we discovered that reduced levels of the lncRNA FEZF1-AS1 inhibited the activation of epithelial‐mesenchymal transition (EMT); the overexpression of orthodenticle homeobox 1 (OTX1) partially rescued the FEZF1-AS1-induced inhibition of protein expression. It indicated that FEZF1-AS1 may play a role in the occurrence and development of CRC by regulating the FEZF1-AS1/OTX1/EMT pathway. Furthermore, it was reported that FEZF1-AS1 is located in both the nucleus and cytoplasm of HCT116 cells. Dual-luciferase reporter assays verified that FEZF1-AS1 directly binds miR-30a-5p and negatively regulated each other. Further, we showed that 5′-nucleotidase ecto (NT5E) is a direct target of miR-30a-5p, and the inhibition of miR-30a-5p expression partially rescued the inhibitory effect of FEZF1-AS1 on NT5E. Our results indicated that the mechanism by which FEZF1-AS1 positively regulates the expression of NT5E is through sponging miR-30a-5p. Our study demonstrated that lncRNA FEZF1-AS1 is involved in the development of CRC and may serve as a diagnostic and therapeutic target for CRC patients.

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