scholarly journals P8‐188: The inhibitory effect of pemetrexed disodium heptahydrate on the growth of KRAS‐dependent A549 cells

Respirology ◽  
2021 ◽  
Vol 26 (S3) ◽  
pp. 361-361
2021 ◽  
Author(s):  
Md Mohiuddin ◽  
Hideharu Kimura ◽  
Takashi Sone ◽  
Satoshi Watanabe ◽  
Hiroki Matsuoka ◽  
...  

2021 ◽  
pp. 37-40

Purpose: The rapid growth, morbidity and mortality of lung cancer and the lack of effective treatment have attracted great interest from researchers to find new cancer treatments aimed at the effect of gossypine on cell proliferation and apoptosis of A549 cells. The most used of these products are flavonoids. Gossypin is a potential chemo preventive and therapeutic agent for lung cancer. Material and Method: We investigated the effect of Gossypin anticancer activity on A549 cell proliferation with MTT method, depending on dose and time. In addition, mRNA expression levels of the apoptotic markers caspase-3 (CAS-3) and caspase-9 (CAS-9) were investigated by real-time PCR. In our study, six groups were used as control, gossypin (10, 20, 40 μM), cisplatin 5 μg/mL and cisplatin 5 μg/mL+gossypin 40 μM combine concentrations. The proliferative and antiapoptotic effects of gossypin at 24, 48 and 72 hours were investigated. Results were analyzed and presented as cell viability (%). Results: In our results, it was determined that gossypin especially at a dose of 40 μM and at 72 hours showed almost as much effect on A549 cells, but the highest inhibitory effect was seen in the 40 combined group of cisplatin 5 μg / mL + gossypin. In addition, gossypin caused a significant increase in apoptosis genes (CASP-3, CASP-9) compared to control. Conclusion: Our study showed that gossypin significantly increases the chemosensitivity of cisplatin. Based on this, it is predicted that gossypin can be used as a supportive therapy that increases the effectiveness of anticancer agents. However, more detailed research should be done for this.


2007 ◽  
Vol 19 (4) ◽  
pp. 283-286 ◽  
Author(s):  
Xiao-hua Wang ◽  
Yuan-qin Yin ◽  
Cheng-guang Sui ◽  
Fan-dong Meng ◽  
Ping Ma ◽  
...  
Keyword(s):  

2015 ◽  
Vol 6 ◽  
pp. 1306-1318 ◽  
Author(s):  
Maria J Ramalho ◽  
Joana A Loureiro ◽  
Bárbara Gomes ◽  
Manuela F Frasco ◽  
Manuel A N Coelho ◽  
...  

Poly(lactic-co-glycolic acid) (PLGA) nanoparticles were studied as drug delivery vehicles for calcitriol, the active form of vitamin D3. In vitro effects of calcitriol encapsulated in PLGA nanoparticles were evaluated with respect to free calcitriol on human pancreatic cell lines, S2-013 and hTERT-HPNE, and the lung cancer cell line A549. Encapsulated calcitriol retained its biological activity, reducing the cell growth. Cytotoxicity assays demonstrated that encapsulation of calcitriol enhanced its inhibitory effect on cell growth at a concentration of 2.4 μM for the S2-013 cells (91%) and for A549 cells (70%) comparared to the free calcitriol results. At this concentration the inhibitory effect on nontumor cells (hTERT-HPNE) decreased to 65%. This study highlights the ability of PLGA nanoparticles to deliver vitamin D3 into cancer cells, with major effects regarding cancer cell cycle arrest and major changes in the cell morphological features.


2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Cuixia Wen ◽  
Yun Zhou ◽  
Chong Zhou ◽  
Yifan Zhang ◽  
Xiang Hu ◽  
...  

Curcumin, the principal polyphenolic curcuminoid, has been reported in numerous studies for its antitumor effect in a series of cancers. It is also reported that curcumin possesses radiosensitization effect in some cancers. However, the poor solubility and unsatisfied bioavailability of curcumin significantly undermine its potential application. Here we prepared curcumin loaded nanoparticles by employing PVP-PCL as drug carrier. Characterization studies indicated the satisfied drug loading efficiency and a sustained in vitro release pattern. Quantification uptake study showed that the uptake efficiency of Cum-NPs by lung cancer cells was time- and dose-dependent. In vitro anticancer study demonstrated the superior cytotoxic effect of Cum-NPs with stronger apoptotic induction over free Cum. Most importantly, there is almost no report on the radiosensitization effect of curcumin loaded nanoparticles. Here, Cum-NPs led to more inhibition of the colony forming ability of A549 cells as compared to the equivalent concentration of free Cum as shown in clonogenic assay. Furthermore, Cum-NPs are much more effective in enhancing the tumor growth inhibitory effect of radiation therapy in a A549 xenograft model. Therefore, results from the current study seem to be the first report on the radiosensitization effect of Cum-NPs and paved the way for a curcumin nanodrug delivery system as a potential radiation adjuvant.


2011 ◽  
Vol 286 (41) ◽  
pp. 35499-35508 ◽  
Author(s):  
Wan-Lin Liao ◽  
Wei-Chiao Wang ◽  
Wen-Chang Chang ◽  
Joseph T. Tseng

The activation of cytosolic phospholipase A2α (cPLA2α) plays an important role in initiating the inflammatory response. The regulation of cPLA2α mRNA turnover has been proposed to control cPLA2α gene expression under cytokine and growth factor stimulation. However, the detailed mechanism is still unknown. In this report, we have demonstrated that the cPLA2α mRNA stability was increased under IL-1β treatment in A549 cells. By using EMSAs, HuR was identified as binding with the cPLA2α mRNA 3′-UTR, and the binding region was located at nucleotides 2716–2807, a fragment containing AUUUA flanked by U-rich sequences. IL-1β treatment enhanced the association of cPLA2α mRNA with cytosolic HuR. The reduction of HuR expression by RNA interference technology inhibited IL-1β-induced cPLA2α mRNA and protein expression. Furthermore, blocking the p38 MAPK signaling pathway with SB203580 abolished the effect of IL-1β-induced cPLA2α gene expression. Phosphorylation at residue Thr-118 of HuR is crucial in regulating the interaction between HuR and its target mRNAs. Mutation of HuR Thr-118 reduced the association between HuR and cPLA2α mRNA under IL-1β treatment. This inhibitory effect was also observed in binding with COX-2 mRNA. This result indicated that p38 MAPK-mediated Thr-118 phosphorylation may play a key role in regulating the interaction of HuR with its target mRNAs in inflammation.


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