scholarly journals Anticancer Potentials of Root Extract ofPolygala senegaand Its PLGA Nanoparticles-Encapsulated Form

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Saili Paul ◽  
Soumya Sundar Bhattacharyya ◽  
Naoual Boujedaini ◽  
Anisur Rahman Khuda-Bukhsh

Ethanolic extract ofPolygala senega(EEPS) had little or no cytotoxic effects on normal lung cells, but caused cell death and apoptosis to lung cancer cell line A549. In the present paper, ethanolic root extract ofP. senega(EEPS) was nanoencapsulated (size: 147.7 nm) by deploying a biodegradable poly-(lactic-co-glycolic) acid (PLGA). The small size of the NEEPS resulted in an enhanced cellular entry and greater bioavailability. The growth of cancer cells was inhibited better by NEEPS than EEPS. Both EEPS and NEEPS induced apoptosis of A549 cells, which was associated with decreased expression of survivin, PCNA mRNA, and increased expression of caspase-3, p53 mRNAs of A549 cells. The results show that the anticancer potential of the formulation of EEPS-loaded PLGA nanoparticles was more effective than EEPS per se, probably due to more aqueous dispersion after nanoencapsulation. Therefore, nanoencapsulated ethanolic root extract ofP. senegamay serve as a potential chemopreventive agent against lung cancer.

Molecules ◽  
2020 ◽  
Vol 25 (1) ◽  
pp. 231 ◽  
Author(s):  
Juthathip Poofery ◽  
Patompong Khaw-on ◽  
Subhawat Subhawa ◽  
Bungorn Sripanidkulchai ◽  
Apichat Tantraworasin ◽  
...  

The incidence of lung cancer has increased while the mortality rate has continued to remain high. Effective treatment of this disease is the key to survival. Therefore, this study is a necessity in continuing research into new effective treatments. In this study we determined the effects of three different Thai herbs on lung cancer. Bridelia ovata, Croton oblongifolius, and Erythrophleum succirubrum were extracted by ethyl acetate and 50% ethanol. The cytotoxicity was tested with A549 lung cancer cell line. We found four effective extracts that exhibited toxic effects on A549 cells. These extracts included ethyl acetate extracts of B. ovata (BEA), C. oblongifolius (CEA), and E. succirubrum (EEA), and an ethanolic extract of E. succirubrum (EE). Moreover, these effective extracts were tested in combination with chemotherapeutic drugs. An effective synergism of these treatments was found specifically through a combination of BEA with methotrexate, EE with methotrexate, and EE with etoposide. Apoptotic cell death was induced in A549 cells by these effective extracts via the mitochondria-mediated pathway. Additionally, we established primary lung cancer and normal epithelial cells from lung tissue of lung cancer patients. The cytotoxicity results showed that EE had significant potential to be used for lung cancer treatment. In conclusion, the four effective extracts possessed anticancer effects on lung cancer. The most effective extract was found to be E. succirubrum (EE).


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.


2020 ◽  
Vol 10 (3) ◽  
pp. 109 ◽  
Author(s):  
Hee Sung Chae ◽  
Minchan Gil ◽  
Subbroto Kumar Saha ◽  
Hee Jeung Kwak ◽  
Hwan-Woo Park ◽  
...  

Lung cancer remains the most dangerous type of cancer despite recent progress in therapeutic modalities. Development of prognostic markers and therapeutic targets is necessary to enhance lung cancer patient survival. Sestrin family genes (Sestrin1, Sestrin2, and Sestrin3) are involved in protecting cells from stress. In particular, Sestrin2, which mainly protects cells from oxidative stress and acts as a leucine sensor protein in mammalian target of rapamycin (mTOR) signaling, is thought to affect various cancers in different ways. To investigate the role of Sestrin2 expression in lung cancer cells, we knocked down Sestrin2 in A549, a non-small cell lung cancer cell line; this resulted in reduced cell proliferation, migration, sphere formation, and drug resistance, suggesting that Sestrin2 is closely related to lung cancer progression. We analyzed Sestrin2 expression in human tissue using various bioinformatic databases and confirmed higher expression of Sestrin2 in lung cancer cells than in normal lung cells using Oncomine and the Human Protein Atlas. Moreover, analyses using Prognoscan and KMplotter showed that Sestrin2 expression is negatively correlated with the survival of lung cancer patients in multiple datasets. Co-expressed gene analysis revealed Sestrin2-regulated genes and possible associated pathways. Overall, these data suggest that Sestrin2 expression has prognostic value and that it is a possible therapeutic target in lung cancer.


2020 ◽  
Author(s):  
gwan woo Ku ◽  
Yujin Kang ◽  
Seong-Lan Yu ◽  
Joonghoon Park ◽  
Sejin Park ◽  
...  

Abstract Background: lncRNAs have important roles in regulating cancer biology. Accumulating evidence has established a link between the dysregulation of lncRNAs and microRNA in cancer progression. In previous studies, miR-7-5p has been found to be significantly down-regulated in mesenchymal-like lung cancer cell lines and directly regulated EGFR. In this work, we investigated the lncRNA partner of miR-7-5p in the progression of lung cancer.Methods: We investigated the expression of miR-7-5p and the lncRNA after transfection with an miR-7-5p mimics using a microarray. The microarray results were validated using quantitative real time-polymerase Chain Reaction (qRT-PCR). The regulatory effects of lncRNA on miR-7-5p and its target were evaluated by changes in the expression of miR-7-5p after transfection with siRNAs for lncRNA and the synthesis of full-length lncRNA. The effect of miR-7-5p on lncRNA and the miRNA target was evaluated after transfection with miRNA mimic and inhibitor. The role of lncRNA in cancer progression was determined using invasion and migration assays. The level of lncRNA and EGFR in lung cancer and normal lung tissue was analyzed using TCGA data.Results: We found that LINC00240 was downregulated in lung cancer cell line after miR-7-5p transfection with an miR-7-5p mimic. Further investigations revealed that the knockdown of LINC00240 induced the overexpression of miR-7-5p. The overexpression of miR-7-5p diminished cancer invasion and migration. The EGFR expression was down regulated after siRNA treatment for LINC00240. Silencing LINC00240 suppressed the invasion and migration of lung cancer cells, whereas LINC00240 overexpression exerted the opposite effect. The lower expression of LINC00240 in squamous lung cancer was analyzed using TCGA data.Conclusions: Taken together, LINC00240 acted as a sponge for miR-7-5p and induced the overexpression of EGFR. LINC00240 may represent a potential target for the treatment of lung cancer.


2019 ◽  
Vol 22 ◽  
pp. 101381
Author(s):  
Suganya Mani ◽  
Karthik Natesan ◽  
Kavitha Shivaji ◽  
Mythili Gnanamangai Balasubramanian ◽  
Ponmurugan Ponnusamy

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Gwan Woo Ku ◽  
Yujin Kang ◽  
Seong-Lan Yu ◽  
Joonghoon Park ◽  
Sejin Park ◽  
...  

Abstract Background lncRNAs have important roles in regulating cancer biology. Accumulating evidence has established a link between the dysregulation of lncRNAs and microRNA in cancer progression. In previous studies, miR-7-5p has been found to be significantly down-regulated in mesenchymal-like lung cancer cell lines and directly regulated EGFR. In this work, we investigated the lncRNA partner of miR-7-5p in the progression of lung cancer. Methods We investigated the expression of miR-7-5p and the lncRNA after transfection with an miR-7-5p mimics using a microarray. The microarray results were validated using quantitative real time-polymerase Chain Reaction (qRT-PCR). The regulatory effects of lncRNA on miR-7-5p and its target were evaluated by changes in the expression of miR-7-5p after transfection with siRNAs for lncRNA and the synthesis of full-length lncRNA. The effect of miR-7-5p on lncRNA and the miRNA target was evaluated after transfection with miRNA mimic and inhibitor. The role of lncRNA in cancer progression was determined using invasion and migration assays. The level of lncRNA and EGFR in lung cancer and normal lung tissue was analyzed using TCGA data. Results We found that LINC00240 was downregulated in lung cancer cell line after miR-7-5p transfection with an miR-7-5p mimic. Further investigations revealed that the knockdown of LINC00240 induced the overexpression of miR-7-5p. The overexpression of miR-7-5p diminished cancer invasion and migration. The EGFR expression was down regulated after siRNA treatment for LINC00240. Silencing LINC00240 suppressed the invasion and migration of lung cancer cells, whereas LINC00240 overexpression exerted the opposite effect. The lower expression of LINC00240 in squamous lung cancer was analyzed using TCGA data. Conclusions Taken together, LINC00240 acted as a sponge for miR-7-5p and induced the overexpression of EGFR. LINC00240 may represent a potential target for the treatment of lung cancer.


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