scholarly journals SP-8356, a (1S)-(-)-Verbenone Derivative, Inhibits the Growth and Motility of Liver Cancer Cells by Regulating NF-κB and ERK Signaling

2021 ◽  
Author(s):  
Dong Hwi Kim ◽  
Hyo Jeong Yong ◽  
Sunam Mander ◽  
Huong Thi Nguyen ◽  
Lan Phuong Nguyen ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Erk Signaling ◽  
Liver Cancer Cells

Inhibition of PI3K/Akt and ERK signaling decreases visfatin-induced invasion in liver cancer cells

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Candace Miethe ◽  
Linda Torres ◽  
Megan Zamora ◽  
Ramona S. Price
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Fatty Acid Synthase ◽  
Erk Signaling ◽  
Ros Production ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Liver Cancer Cells ◽  
Phosphorylated Akt ◽  
Erk Inhibition

Abstract Objectives Visfatin is found in adipose tissue and is referred to as nicotinamide phosphoribosyltransferase (Nampt). Visfatin has anti-apoptotic, proliferative, and metastatic properties and may mediate its effects via ERK and PI3K/Akt signaling. Studies have yet to determine whether inhibition of kinase signaling will suppress visfatin-induced liver cancer. The purpose of this study was to determine which signaling pathways visfatin may promote liver cancer progression. Methods HepG2 and SNU-449 liver cancer cells were exposed to visfatin with or without ERK or PI3K/Akt inhibitor, or both inhibitors combined. These processes that were assessed: proliferation, reactive oxygen species (ROS), lipogenesis, invasion, and matrix metalloproteinase (MMP). Results Inhibition of PI3K/Akt and combination of inhibitors suppressed visfatin-induced viability. ERK inhibition in HepG2 cells decreased visfatin-induced proliferation. ERK inhibitor alone or in combination with PI3K inhibitors effectively suppressed MMP-9 secretion and invasion in liver cancer cells. PI3K and ERK inhibition and PI3K inhibition alone blocked visfatin’s ROS production in SNU-449 cells. These results corresponded with a decrease in phosphorylated Akt and ERK, β-catenin, and fatty acid synthase. Conclusions Akt and ERK inhibition differentially regulated physiological changes in liver cancer cells. Inhibition of Akt and ERK signaling pathways suppressed visfatin-induced invasion, viability, MMP-9 activation, and ROS production.

scholarly journals Influence of miR‑101 on proliferation of liver cancer cells through the MAPK/ERK signaling pathway

2019 ◽  
Author(s):  
Xuan Meng ◽  
Yong Shi ◽  
Xin Xiang ◽  
Chonghui Li ◽  
Xinlan Ge ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Liver Cancer Cells

Panobinostat treatment determines oncogenic miRNAs down-regulation in liver cancer cells

2012 ◽  
Vol 50 (01) ◽  
Author(s):  
A Henrici ◽  
R Montalbano ◽  
K Quint ◽  
M Ocker ◽  
P Di Fazio
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Down Regulation ◽  
Liver Cancer Cells ◽  
Oncogenic Mirnas

HBV-Encoded miR-2 Functions as an Oncogene by Downregulating TRIM35 But Upregulating RAN in Liver Cancer Cells

2019 ◽  
Author(s):  
Lili Yao ◽  
Zhen-hua Sui ◽  
Yan-Kun Liu ◽  
Hong Xie ◽  
Hui-jie Gao ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Liver Cancer Cells

Titanium Oxide Nanoparticles Improve the Chemotherapeutic Action of Erlotinib in Liver Cancer Cells

2020 ◽  
Vol 16 (4) ◽  
pp. 337-343
Author(s):  
Shaimaa E. Abdel-Ghany ◽  
Eman El-Sayed ◽  
Nour Ashraf ◽  
Nada Mokhtar ◽  
Amany Alqosaibi ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Titanium Oxide ◽  
Phase Distribution ◽  
Oxide Nanoparticles ◽  
Titanium Oxide Nanoparticles ◽  
Liver Cancer Cells ◽  
M Phase ◽  
Apoptosis Detection ◽  
Novel Method

Background: Hepatocellular carcinoma is the second leading cause of cancer-related deaths among other types of cancer due to lack of effective treatments and late diagnosis. Nanocarriers represent a novel method to deliver chemotherapeutic drugs, enhancing their bioavailability and stability. Methods: In the present study, we loaded gold nanoparticles (AuNPs) and titanium oxide nanoparticles (TiO2NPs) with ERL to investigate the efficiency of the formed composite in inducing apoptosis in HepG2 liver cancer cells. Cytotoxicity was assessed using MTT assay and cell phase distribution was assessed by flow cytometry along with apoptosis detection. Results: Data obtained indicated the efficiency of the formed composite to significantly induce cell death and arrest cell cycle and G2/M phase. IRF4 was downregulated after treatment with loaded ERL. Conclusion: Our data showed that loading ERL on TiO2NPs was more efficient than AuNPs. However, both nanocarriers were efficient compared with control.

Precise Electrical Detection of Curcumin Cytotoxicity in Human Liver Cancer Cells

2021 ◽  
Author(s):  
Novi Angeline ◽  
Sung-Sik Choo ◽  
Cheol-Hwi Kim ◽  
Suk Ho Bhang ◽  
Tae-Hyung Kim
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Human Liver ◽  
Electrical Detection ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

Relevance of mitochondrial dysfunction during Sorafenib-induced cell death in liver cancer cells. Role of oxidative and nitrogen reactive species

2021 ◽  
Vol 165 ◽  
pp. 54
Author(s):  
Patricia de la Cruz-Ojeda ◽  
M. Ángeles Rodríguez-Hernández ◽  
Elena Navarro-Villarán ◽  
Paloma Gallego ◽  
Pavla Staňková ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Cancer ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Reactive Species ◽  
Liver Cancer Cells ◽  
Nitrogen Reactive Species

scholarly journals Echinacoside exerts anti-tumor activity via the miR-503-3p/TGF-β1/Smad aixs in liver cancer

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wen Li ◽  
Jing Zhou ◽  
Yajie Zhang ◽  
Jing Zhang ◽  
Xue Li ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Hepg2 Cells ◽  
Luciferase Reporter ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Expression Levels ◽  
Liver Cancer Cells ◽  
Anti Tumor Activity ◽  
Tgf Β1

Abstract Background Echinacoside (ECH) is the main active ingredient of Cistanches Herba, which is known to have therapeutic effects on metastatic tumors. However, the effects of ECH on liver cancer are still unclear. This study was to investigate the effects of ECH on the aggression of liver cancer cells. Methods Two types of liver cancer cells Huh7 and HepG2 were treated with different doses of ECH at different times and gradients. MTT and colony formation assays were used to determine the effects of ECH on the viability of Huh7 and HepG2 cells. Transwell assays and flow cytometry assays were used to detect the effects of ECH treatment on the invasion, migration, apoptosis and cell cycle of Huh7 and HepG2 cells. Western blot analysis was used to detect the effects of ECH on the expression levels of TGF-β1, smad3, smad7, apoptosis-related proteins (Caspase-3, Caspase-8), and Cyto C in liver cancer cells. The relationship between miR-503-3p and TGF-β1 was detected using bioinformatics analysis and Luciferase reporter assay. Results The results showed that ECH inhibited the proliferation, invasion and migration of Huh7 and HepG2 cells in a dose- and time-dependent manner. Moreover, we found that ECH caused Huh7 and HepG2 cell apoptosis by blocking cells in S phase. Furthermore, the expression of miR-503-3p was found to be reduced in liver tumor tissues, but ECH treatment increased the expression of miR-503-3p in Huh7 and HepG2 cells. In addition, we found that TGF-β1 was identified as a potential target of miR-503-3p. ECH promoted the activation of the TGF-β1/Smad signaling pathway and increased the expression levels of Bax/Bcl-2. Moreover, ECH could trigger the release of mitochondrial Cyto C, and cause the reaction Caspases grade. Conclusions This study demonstrates that ECH exerts anti-tumor activity via the miR-503-3p/TGF-β1/Smad aixs in liver cancer, and provides a safe and effective anti-tumor agent for liver cancer.

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