scholarly journals An Investigation on Cytotoxicity Effect of Putrescine-Sulphur Analogues on Breast Cancer (Mcf-7), Human Lung Adenocarcinoma (A549) and Colorectal Cancer (Hct-8) Cell Lines

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Norsuhana Halim ◽  
Radiah Abdul Ghani ◽  
Adzly Hairee Sahabudin ◽  
Fiona How Ni Fong
Keyword(s):  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Cell Lines ◽  
Human Lung ◽  
Breast Adenocarcinoma ◽  
Normal Cells ◽  
Human Lung Adenocarcinoma ◽  
Adenocarcinoma Cells ◽  
Specific Cancer ◽  
Mcf 7

Introduction: Cancer is one of the global health problems that has a detrimental effect to a person's life. However, chemotherapeutic agents success are subject to the side effects due to lack of specificity in the drug delivery system to cancer cells and an increase risk of systemic toxicity to the normal cells. Polyamine transport system (PTS) is one of the potential pathways for transporting anticancer agent into specific cancer cells. This is due to the upregulation of PTS in cancer cells compared to normal cells for the proliferation activity. The aim of this study was to investigate the cytotoxicity effect of putrescine-sulphur analogues type 1 (PSA-1) and type 2 (PSA-2) on human lung adenocarcinoma cells (A549), human colorectal adenocarcinoma cells (HCT-8) and human breast adenocarcinoma cell (MCF-7). Materials and method: The cytotoxicity effect of newly synthesized PSA-1 and PSA-2 were evaluated on selected cancer cells; MCF-7, A549 and HCT-8 cell lines. The halfmaximal inhibitory concentration (IC50) obtained from tetrazolium bromide (MTT) assay was derived from the dose-response graph for all cell lines. Results: PSA-2 elicited cytotoxicity effect, eventhough the IC50 values were not potent with IC50 of 5.4 mM, 5.2 mM and 7.0 mM for MCF-7/48h, A549/48h and HCT-8/48h, respectively. The PSA-1 compound exhibited cytotoxicity effect in all cell lines, however, the compound failed to induce anti-proliferation at the concentration of 3 mM and above. The cytotoxicity of PSA-2 compound against MCF-7 cell lines showed higher potency compared to A549 and HCT-8 cell lines. Conclusion: It was suggested that PSA-2 compound was able to exert cytotoxicity effect against selected cancer cells, in low potency and is deemed for further investigation to increase its effectiveness against specific cancer cells.

scholarly journals The Cytotoxicity Effect of Spermidine -Sulphur Analogues Type 1 (Ssa-1) And Type 2 (Ssa-2) against Human Lung Adenocarcinoma Cells (A549), Human Colorectal Adenocarcinoma Cells (Hct-8), and Human Breast Adenocarcinoma Cells (Mcf-7)

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Masnizahani binti Jamil ◽  
Radiah Abdul Ghani ◽  
Adzly Hairee Sahabudin ◽  
Fiona How Ni Fong
Keyword(s):  
Cell Lines ◽  
Colorectal Adenocarcinoma ◽  
Human Lung ◽  
Breast Adenocarcinoma ◽  
Human Breast ◽  
Adenocarcinoma Cells ◽  
Human Lung Adenocarcinoma Cells ◽  
Mcf 7

Introduction: Over accumulation of polyamines is one of the causes of cancer because polyamines could promote the cancer cells growth. Due to the lack of specificity and increased reports of side effects in the current cancer treatment, one of the strategies to overcome the challenges is by utilizing polyamines as vectors of known cytotoxic compounds to target the cancer cells. Therefore, this study was aimed to investigate the cytotoxicity effect of Spermidine Sulphur Analogues Type 1 and Type 2 (SSA-1 and SSA-2) against human lung adenocarcinoma cells (A549), human colorectal adenocarcinoma cells (HCT-8) and human breast adenocarcinoma cell (MCF-7).  Materials and method: The cytotoxicity studies of SSA-1 and SSA-2 against in vitro cells: A549, HCT-8, and MCF-7 were carried out by using MTT assay and the IC50 in each cell was determined.  Results: SSA-1 exhibited cytotoxicity effect in all selected cell lines with IC50 between 2.0 mM to 5.3 mM. While SSA-2 also exhibited cytotoxicity effect in all cell lines with IC50 between 0.8 mM to 5.0 mM.  Conclusion: SSA-1 and SSA-2 were cytotoxic against A549, HCT-8, and MCF-7. However, the cytotoxic effect was not potent against these cell lines as a higher concentration of compounds was needed to inhibit the cells growth. Hence, it is suggested that further study on the cytotoxicity effect of SSA-1 and SSA-2 in other cell lines should be conducted and the formulation of the analogues based on sulphur should be amended by conjugating it with selected metal.

scholarly journals Cytotoxic Constituents from the Sclerotia of Poria cocos against Human Lung Adenocarcinoma Cells by Inducing Mitochondrial Apoptosis

Cells ◽  
2018 ◽  
Vol 7 (9) ◽  
pp. 116 ◽  
Author(s):  
Seulah Lee ◽  
Seul Lee ◽  
Hyun-Soo Roh ◽  
Seong-Soo Song ◽  
Rhim Ryoo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Human Lung ◽  
Bioactive Constituents ◽  
Human Lung Adenocarcinoma ◽  
Adenocarcinoma Cells ◽  
Human Lung Adenocarcinoma Cells ◽  
P53 Status ◽  
Lung Adenocarcinoma Cells

Previous studies have revealed the antitumor potential of Poria cocos Wolf against a broad spectrum of cancers. However, the biological activity of P. cocos against lung cancer, which is known as the leading cause of cancer mortality worldwide, and its underlying chemical and molecular basis, remain to be investigated. We aimed to evaluate the in vitro cytotoxicity of P. cocos toward human lung adenocarcinoma cells with different p53 statuses, to identify the bioactive constituents of P. cocos, and explicate the molecular mechanisms underlying the cytotoxicity of these constituents in human lung adenocarcinoma cells. An EtOH extract of the sclerotia of P. cocos exhibited cytotoxicity toward four human lung cancer cell lines: A549, H1264, H1299, and Calu-6, regardless of their p53 status. Chemical investigation of the extract resulted in the isolation of two triterpenoids, dehydroeburicoic acid monoacetate (1) and acetyl eburicoic acid (4); a sterol, 9,11-dehydroergosterol peroxide (2); and a diterpenoid, dehydroabietic acid (3). All of the isolated compounds were cytotoxic to the lung adenocarcinoma cell lines, exhibiting IC50 values ranging from 63.6 μM to 171.0 μM at 48 h of treatment. The cytotoxicity of the extract and the isolated compounds were found to be mediated by apoptosis, and accompanied by elevated Bax expression and/or Bcl-2 phosphorylation along with caspase-3 activation. Our data demonstrate that the sclerotium of P. cocos and its four bioactive constituents (1–4) exert cytotoxicity against human lung adenocarcinoma cells, regardless of their p53 status, by inducing apoptosis associated with mitochondrial perturbation, and proposing the potential to employ P. cocos in the treatment of lung cancer.

scholarly journals Gender difference in the activity but not expression of estrogen receptors α and β in human lung adenocarcinoma cells

2006 ◽  
Vol 13 (1) ◽  
pp. 113-134 ◽  
Author(s):  
Susan M Dougherty ◽  
Williard Mazhawidza ◽  
Aimee R Bohn ◽  
Krista A Robinson ◽  
Kathleen A Mattingly ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Normal Lung ◽  
Adenocarcinoma Cell ◽  
Human Lung Adenocarcinoma ◽  
Estrogen Response ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

The higher frequency of lung adenocarcinoma in women smokers than in men smokers suggests a role for gender-dependent factors in the etiology of lung cancer. We evaluated estrogen receptor (ER) α and β expression and activity in human lung adenocarcinoma cell lines and normal lung fibroblasts. Full-length ERα and ERβ proteins were expressed in all cell lines with higher ERβ than ERα. Although estradiol (E2) binding was similar, E2 stimulated proliferation only in cells from females, and this response was inhibited by anti-estrogens 4-hydroxytamoxifen (4-OHT) and ICI 182,780. In contrast, E2 did not stimulate replication of lung adenocarcinoma cells from males and 4-OHT or ICI did not block cell proliferation. Similarly, transcription of an estrogen response element-driven reporter gene was stimulated by E2 in lung adenocarcinoma cells from females, but not males. Progesterone receptor (PR) expression was increased by E2 in two out of five adenocarcinoma cell lines from females, but none from males. E2 decreased E-cadherin protein expression in some of the cell lines from females, as it did in MCF-7 breast cancer cells, but not in the cell lines from males. Thus, ERα and ERβ expression does not correlate with the effect of ER ligands on cellular activities in lung adenocarcinoma cells. On the other hand, coactivator DRIP205 expression was higher in lung adenocarcinoma cells from females versus males and higher in adenocarcinoma cells than in normal human bronchial epithelial cells. DRIP205 and other ER coregulators may contribute to differences in estrogen responsiveness between lung adenocarcinoma cells in females and males.

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