scholarly journals In silico and in vitro Studies on Lyngbya majuscula using against Lung Cancer Cell Line (A549)

2018 ◽  
Vol 10 (3) ◽  
pp. 421-428 ◽  
Author(s):  
Sangeetha Muniaraj ◽  
Vijayakumar Subramanian ◽  
Prabhu Srinivasan ◽  
Manogar Palani
2006 ◽  
Vol 32 (9) ◽  
pp. 441-453 ◽  
Author(s):  
M. Waheed Roomi ◽  
Vadim Ivanov ◽  
Tatiana Kalinovsky ◽  
Aleksandra Niedzwiecki ◽  
Matthias Rath

2008 ◽  
Vol 3 (10) ◽  
pp. 1934578X0800301 ◽  
Author(s):  
Fabiola Salas ◽  
Janne Rojas ◽  
Antonio Morales ◽  
Maria E. Ramos-Nino ◽  
Nelida G. Colmenares

Sesamin extracted from Vismia baccifera var. dealbata was demonstrated to have cytostatic activity on the cancer cell lines tested, particularly the lung cancer cell line, with an IC50 of 1 g/L.


Tumor Biology ◽  
2014 ◽  
Vol 35 (7) ◽  
pp. 7259-7266 ◽  
Author(s):  
Hongmin Wang ◽  
Xiaohong Zhang ◽  
Yuexia Li ◽  
Ruiying Chen ◽  
Songyun Ouyang ◽  
...  

2018 ◽  
Vol 187 (4) ◽  
pp. 1328-1343 ◽  
Author(s):  
Kok-Tong Tan ◽  
Shiming Li ◽  
Yi Rong Li ◽  
Shih-Lung Cheng ◽  
Sheng-Hao Lin ◽  
...  

2019 ◽  
Vol 16 (4) ◽  
pp. 338-349
Author(s):  
Arielis Rodríguez-Ulloa ◽  
Yassel Ramos ◽  
Aniel Sánchez-Puente ◽  
Yasser Perera ◽  
Alexis Musacchio-Lasa ◽  
...  

Background: CIGB-300 is a pro-apoptotic peptide that abrogates CK2-mediated phosphorylation, and can elicit synergistic interaction in vitro and in vivo when combined with certain anticancer drugs. Objective: The combination of CIGB-300 with cisplatin is studied through data mining and expressionbased proteomics to reveal the molecular basis of this interaction. Cisplatin resistance-associated proteins, which have also been reported as CK2 substrates, were first identified by bioinformatic analyses. Methods: Data from these analyses suggested that the cisplatin resistance phenotype could be directly improved by inhibiting CK2 phosphorylation on specific substrates. Furthermore, 157 proteins were differentially modulated on the NCI-H125 lung cancer cell line in response to CIGB-300, cisplatin or both drugs as determined by LC-MS/MS. Results: The expression of 28 cisplatin resistance-associated proteins was changed when cisplatin was combined with CIGB-300. Overall, the proteins identified are also related to cell survival, cell proliferation and metastasis. Furthermore, the CIGB-300 regulated proteome revealed proteins that were initially involved in the mechanism of action of CIGB-300 and cisplatin as single agents. Conclusion: This is the first report describing the protein array modulated by combining CIGB-300 and cisplatin that will support the rationale for future clinical settings based on a multi-target cancer therapy.


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