scholarly journals Lectin from Pisum fulvum Seeds as in vitro Anticancer and Apoptotic Gene Regulator

2019 ◽  
Vol 70 (4) ◽  
pp. 1490-1495 ◽  
Author(s):  
Abdelrahman Mohamed Yassin ◽  
Nehal Mohamed El-Deeb ◽  
Fahmy Gad Elsaid ◽  
Ali Abdullah Shati ◽  
Gabriela Cioca ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Research Work ◽  
Cell Types ◽  
Carcinoma Cells ◽  
Brdu Incorporation ◽  
Molecular Evidence ◽  
Carbohydrate Binding ◽  
Nuclear Condensation ◽  
Pisum Fulvum

The lectins are non-immune origin carbohydrate-binding proteins. Plant�s lectins are distributed in many species of medicinal plants, family Fabaceae. In this study the safety usage pattern of wild Pisum fulvum lectin was evaluated on different mammalian noncancerous cell types and the anticancer activity was examined on different cancer human cell lines: colorectal adenocarcinoma (Caco-2), hepatocellular carcinoma (HepG2), breast cancer cells (MCF7) and laryngeal carcinoma (Hep-2 cells). Moreover, both morphological and molecular evidence of apoptosis have been detected using both acridine orange/ethidium bromide (AO/EB) stain and RT-qPCR. The results revealed that IC50 of the wild lectin on the noncancerous cells ranged from 19.7 to 2.4 �g protein/mL. In addition, lectin was more potent against HepG2 cells than the other used cells, with inhibition percentages ranged from 68.45 to 90.98 and with cancer cell selectivity index ranged 3.5 to 28.14. The treatment showed 67.6% inhibition of BrdU incorporation in the proliferated hepatocellular carcinoma cells. Furthermore, HepG2-lectin treated cells showed obvious nuclear condensation after 48 h of treatment with ability to down-regulate the expression of BCL2 and BAX and to up-regulate the expression of Ikab gene. The results obtained in this research work clearly indicated the Pisum fulvum lectin could be a promising potential anticancer agent.

scholarly journals Bioinformatics Profiling of Five Immune-Related lncRNAs for a Prognostic Model of Hepatocellular Carcinoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Fahong Wu ◽  
Hangzhi Wei ◽  
Guiyuan Liu ◽  
Youcheng Zhang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Prognostic Model ◽  
Cox Regression ◽  
Malignant Tumors ◽  
Cell Types ◽  
Carcinoma Cells ◽  
Cox Regression Analysis ◽  
Rna Transcripts ◽  
Specificity And Sensitivity

Hepatocellular carcinoma (HCC), one of the most common tumors worldwide, has the fifth highest mortality rate, which is increasing every year. At present, many studies have revealed that immunotherapy has an important effect on many malignant tumors. The main purpose of our research was to verify and establish a new immune-related lncRNA model and to explore the potential immune mechanisms. We analysed the pathways and mechanisms of immune-related lncRNAs by bioinformatics analysis, screened key lncRNAs based on Cox regression analysis, and determined the characteristics of the immune-related lncRNAs. On this basis, a predictive model was established. Through a comparison of specificity and sensitivity, we found that the constructed model was superior to the known markers of HCC. Then, the cell types were identified by the relative subgroup (CIBERSORT) algorithm for RNA transcripts. A signature model was eventually constructed, and we proved that it was a survival factor for HCC. Moreover, five kinds of immune cells were significantly positively correlated with the signature. The results indicated that these five kinds of lncRNAs may be related to the immune infiltration of hepatocellular carcinoma. To verify these findings, we selected the top coexpressed lncRNA, AC099850.3, for further study. We found that AC099850.3 could promote the migration and proliferation of hepatocellular carcinoma cells in vitro. RT-PCR experiments found that AC099850.3 could promote the expression of the cell cycle molecules BUB1, CDK1, PLK1, and TTK, and western blotting to prove that the expression of the molecules CD155 and PD-L1 was inhibited in the interference group. In conclusion, we used five kinds of immune-related lncRNAs to construct prognostic signatures to explore the mechanism, which provides a new way to study therapies for HCC.

scholarly journals Retraction: MiR-206 reduced the malignancy of hepatocellular carcinoma cells in vitro by inhibiting MET and CTNNB1 gene expressions

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4439-4439
Author(s):  
Laura Fisher
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Gene Expressions ◽  
Hepatocellular Carcinoma Cells ◽  
Ctnnb1 Gene

Retraction of ‘MiR-206 reduced the malignancy of hepatocellular carcinoma cells in vitro by inhibiting MET and CTNNB1 gene expressions’ by Qiang He et al., RSC Adv., 2019, 9, 1717–1725, DOI: 10.1039/C8RA09229J

scholarly journals Sirt1 deacetylates and stabilizes p62 to promote hepato-carcinogenesis

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Lifeng Feng ◽  
Miaoqin Chen ◽  
Yiling Li ◽  
Muchun Li ◽  
Shiman Hu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Overall Survival ◽  
Cell Growth ◽  
Knockout Mice ◽  
Liver Tumors ◽  
Underlying Mechanism ◽  
Carcinoma Cells ◽  
Conditional Knockout

Abstractp62/SQSTM1 is frequently up-regulated in many cancers including hepatocellular carcinoma. Highly expressed p62 promotes hepato-carcinogenesis by activating many signaling pathways including Nrf2, mTORC1, and NFκB signaling. However, the underlying mechanism for p62 up-regulation in hepatocellular carcinoma remains largely unclear. Herein, we confirmed that p62 was up-regulated in hepatocellular carcinoma and its higher expression was associated with shorter overall survival in patients. The knockdown of p62 in hepatocellular carcinoma cells decreased cell growth in vitro and in vivo. Intriguingly, p62 protein stability could be reduced by its acetylation at lysine 295, which was regulated by deacetylase Sirt1 and acetyltransferase GCN5. Acetylated p62 increased its association with the E3 ligase Keap1, which facilitated its poly-ubiquitination-dependent proteasomal degradation. Moreover, Sirt1 was up-regulated to deacetylate and stabilize p62 in hepatocellular carcinoma. Additionally, Hepatocyte Sirt1 conditional knockout mice developed much fewer liver tumors after Diethynitrosamine treatment, which could be reversed by the re-introduction of exogenous p62. Taken together, Sirt1 deacetylates p62 at lysine 295 to disturb Keap1-mediated p62 poly-ubiquitination, thus up-regulating p62 expression to promote hepato-carcinogenesis. Therefore, targeting Sirt1 or p62 is a reasonable strategy for the treatment of hepatocellular carcinoma.

scholarly journals CRISPR/Cas9-mediated genome engineering of CXCR4 decreases the malignancy of hepatocellular carcinoma cells in vitro and in vivo

2017 ◽  
Vol 37 (6) ◽  
pp. 3565-3571 ◽  
Author(s):  
Xiaoli Wang ◽  
Wenmei Zhang ◽  
Yan Ding ◽  
Xingrong Guo ◽  
Yahong Yuan ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Genome Engineering ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells
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