Anti-proliferative activity of the combination of salan Ti(iv) complexes with other organic and inorganic anticancer drugs against HT-29 and NCI-H1229 cells: synergism with cisplatin

RSC Advances ◽  
2015 ◽  
Vol 5 (11) ◽  
pp. 7874-7879 ◽  
Author(s):  
Nitzan Ganot ◽  
Boris Redko ◽  
Gary Gellerman ◽  
Edit Y. Tshuva

Cytotoxic salan Ti(iv) complex demonstrated synergism with cisplatin in vitro toward human colon and lung cancer cells at various ratios.

2005 ◽  
Vol 222 (2) ◽  
pp. 183-193 ◽  
Author(s):  
Yeung-Leung Cheng ◽  
Shih-Chun Lee ◽  
Shinn-Zong Lin ◽  
Wen-Liang Chang ◽  
Yi-Lin Chen ◽  
...  

2017 ◽  
Vol 79 (2) ◽  
Author(s):  
Syazwan Aizad ◽  
Nadzirah Mohd Khairiri ◽  
Badrul Hisham Yahaya ◽  
Saiful Irwan Zubairi

Centella asiatica or pegaga is one of the botanical plants that consists of many phytochemicals and is known for being able to offer various effects on wound healing, as well as functioning as an antioxidant and anticancer property. Therefore, this study was carried out to determine the efficacy of Centella asiatica water and alcohol-based extracts on the anti-proliferative activity of human lung cancer cells (A549) and normal fibroblast (IMR90) by mean of in vitro 3-D cell culture system. A porous 3-D scaffold was fabricated from poly(hydroxybutyrate-co-hydroxyvalerate) (PHBV) using solvent-casting particulate-leaching (SCPL) process. Antioxidant analysis (total phenolic content (TPC), DPPH and FRAP assays) was conducted prior to the 3-D cell culture study. The results showed that the extract contained 7.50 ± 1.10 mg/ml of asiaticoside and 0.74 ± 0.24 mg/ml of madecassoside. These bio-active compounds were believed to inhibit the proliferation of cancer cells (A549). The availability of phenolic compounds in the extract (TPC: 10133 ± 119.30 mg/100 g) had proven that the antioxidant properties existed. Moreover, the other values obtained from the antioxidant analysis revealed its capacity as a good source of antioxidant (DPPH: 87 ± 1.0%; FRAP: 127 ± 14.98 mg/100 g). Next, the lung cancer cells (A549) were cultured using a two-dimensional (2-D) system to generate the IC50 value of 5.75 ± 1.0 µg/ml. The A549 cell viability (MTS assay)  after a 3-day incubation exhibited a good sign of mortality  for the both treated models ranging from 55% to 70% as compared to control one (without treatment) (p>0.05). However, when the extract was exposed to a normal fibroblast IMR90, the cell growth of the both treated models exhibited an almost 2-fold greater cell numbers than that of the untreated models (p<0.05) indicating that the extract did not possess any possible threat to a normal and healthy cell. Therefore, the use of Centella asiatica extracts in terminating cancer cells has been proven to be able to inhibit cell growth (greater than 40%) in just 3 days of incubation. 


Author(s):  
Jiongwei Pan ◽  
Gang Huang ◽  
Zhangyong Yin ◽  
Xiaoping Cai ◽  
Enhui Gong ◽  
...  

AbstractSignificantly high-expressed circFLNA has been found in various cancer cell lines, but not in lung cancer. Therefore, this study aimed to explore the role of circFLNA in the progression of lung cancer. The target gene of circFLNA was determined by bioinformatics and luciferase reporter assay. Viability, proliferation, migration, and invasion of the transfected cells were detected by CCK-8, colony formation, wound-healing, and transwell assays, respectively. A mouse subcutaneous xenotransplanted tumor model was established, and the expressions of circFLNA, miR-486-3p, XRCC1, CYP1A1, and related genes in the cancer cells and tissues were detected by RT-qPCR, Western blot, or immunohistochemistry. The current study found that miR-486-3p was low-expressed in lung cancer. MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells. Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic. Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. However, overexpressed XRCC1 and CYP1A1 reversed the inhibitory effect of miR-486-3p mimic on cancer cells and tumors. In conclusion, circFLNA acted as a sponge of miR-486-3p to promote the proliferation, migration, and invasion of lung cancer cells in vitro and in vivo by regulating XRCC1 and CYP1A1.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ronggang Luo ◽  
Yi Zhuo ◽  
Quan Du ◽  
Rendong Xiao

Abstract Background To detect and investigate the expression of POU domain class 2 transcription factor 2 (POU2F2) in human lung cancer tissues, its role in lung cancer progression, and the potential mechanisms. Methods Immunohistochemical (IHC) assays were conducted to assess the expression of POU2F2 in human lung cancer tissues. Immunoblot assays were performed to assess the expression levels of POU2F2 in human lung cancer tissues and cell lines. CCK-8, colony formation, and transwell-migration/invasion assays were conducted to detect the effects of POU2F2 and AGO1 on the proliferaion and motility of A549 and H1299 cells in vitro. CHIP and luciferase assays were performed for the mechanism study. A tumor xenotransplantation model was used to detect the effects of POU2F2 on tumor growth in vivo. Results We found POU2F2 was highly expressed in human lung cancer tissues and cell lines, and associated with the lung cancer patients’ prognosis and clinical features. POU2F2 promoted the proliferation, and motility of lung cancer cells via targeting AGO1 in vitro. Additionally, POU2F2 promoted tumor growth of lung cancer cells via AGO1 in vivo. Conclusion We found POU2F2 was highly expressed in lung cancer cells and confirmed the involvement of POU2F2 in lung cancer progression, and thought POU2F2 could act as a potential therapeutic target for lung cancer.


2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.


Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 79
Author(s):  
Hengju Ge ◽  
Di Zhang ◽  
Muran Shi ◽  
Xiaoyuan Lian ◽  
Zhizhen Zhang

In 2019, streptoglutarimide H (SGH) was characterized as a new glutarimide from the secondary metabolites produced by a marine-derived actinomycete Streptomyces sp. ZZ741 and shown to have in vitro antiglioma activity. However, the antiproliferative activity and potential mechanism of SGH against lung cancer cells have not yet been characterized. This study demonstrated that SGH significantly inhibited the proliferation of different lung cancer cells. In terms of mechanism of action, SGH downregulated cell cycle- and nucleotide synthesis-related proteins to block cell cycle at G0/G1 phase, reduced the expression levels of glycolytic metabolic enzymes to inhibit glycolysis, and downregulated the important cancer transcription factor c-Myc and the therapeutic target deubiquitinase USP28. Potent anticancer activity and multiple mechanisms indicated SGH to be a novel antitumor compound against lung cancer cells.


2010 ◽  
Vol 43 (10) ◽  
pp. 1001-1009 ◽  
Author(s):  
A.O. Santos ◽  
J.P. Pereira ◽  
M.C. Pedroso de Lima ◽  
S. Simões ◽  
J.N. Moreira

Sign in / Sign up

Export Citation Format

Share Document