scholarly journals In VivoAnticancer Activity ofBasella albaLeaf and Seed Extracts against Ehrlich's Ascites Carcinoma (EAC) Cell Line

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Md. Shihabul Islam ◽  
Md. Sifat Rahi ◽  
Chowdhury Arif Jahangir ◽  
Md Habibur Rahman ◽  
Israt Jerin ◽  
...  
Keyword(s):  
Side Effects ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Line ◽  
Seed Extract ◽  
Morphological Alteration ◽  
Pcr Analysis ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition ◽  
Seed Extracts

Cancer is a class of diseases characterized by uncontrolled cell growth. The current treatment options of cancer are radiotherapy, chemotherapy, hormone therapy, and surgery, where all of them have unpleasant side effects. Due to their adverse side effects, it is challenging to develop new drug for cancer treatment. Hence, the scientists are trying to seek for noble compounds from natural sources to treat cancer. Therefore, in the present investigation, a widely consumable vegetableBasella albawas subjected to evaluate its antiproliferative effect along with molecular signaling of apoptosis in Ehrlich ascites carcinoma (EAC) cell line. Cell growth inhibition was determined by haemocytometer whereas apoptosis of cancer cells were studied by florescence microscope using Hoechst-33342 stain and result was supported by DNA fragmentation and certain cancer related genes expression through PCR analysis.B. albaleaf and seed extract exhibit a considerable scavenging activity in comparison to a standard antioxidant BHT. Moreover, the leaf and seed extracts were able to agglutinate 2% RBC of goat blood at minimum 12.5μg/ml and 50.0μg/ml concentration, respectively. A significant cytotoxic activity was also found in both leaf and seed extract. In haemocytometic observation, the leaf and seed extracts exhibit about 62.54±2.41% and 53.96±2.34% cell growth inhibition, respectively, whereas standard anticancer drug Bleomycin showed 79.43±1.92% growth inhibition. Morphological alteration under fluorescence microscope showed nuclear condensation and fragmentation which is the sign of apoptosis. Apoptosis induction was also confirmed by DNA laddering in leaf and seed treated EAC cells. Upregulation of the tumor suppressor gene P53and downregulation of antiapoptotic gene Bcl-2 enumerate apoptosis induction. Therefore, current study manifested that leaf and seed extracts ofB. albahave antiproliferative activity against EAC cell line and can be a potent source of anticancer agents to treat cancer.

scholarly journals δ-Tocopherol Enhances Docetaxel-Induced Growth Inhibition and Apoptosis in Ovarian Cancer SKOV3 Cells

2021 ◽  
Vol 16 (3) ◽  
pp. 1934578X2110022
Author(s):  
Hongjuan Chai ◽  
Jugang Wu ◽  
Junlei Liu ◽  
Ting Liu ◽  
Qing Ren ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Side Effects ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Apoptosis ◽  
Induction Effect ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition ◽  
Skov3 Cells

Docetaxel is the first-line chemotherapeutic drug for ovarian cancer. However, its clinical use is limited owing to its serious side effects. Therefore, it is of great clinical significance to enhance the efficacy of docetaxel at lower doses in a less-toxic manner. In this study, we investigated whether δ-tocopherol could enhance the anti-tumor effects of docetaxel on ovarian cancer SKOV3 cells in vitro. For docetaxel and δ-tocopherol, IC50 values of 1.89 nM and 11.41 µM, respectively, were obtained, in SKOV3 cells. The combination of δ-tocopherol and docetaxel had a synergistic cell growth inhibition effect, with lower cell viability and more cell arrest at the S phase compared to either δ-tocopherol or docetaxel alone. In addition, the combination of δ-tocopherol and docetaxel had a synergistic cell apoptosis induction effect, with more apoptotic cells and reduced anti-apoptotic protein expression compared to either δ-tocopherol or docetaxel alone. Furthermore, we identified 3 hoursub genes (CAT, EP300, CREBBP), which predicted the prognosis of ovarian cancer, which correlated with δ-tocopherol and docetaxel. In conclusion, the combination of δ-tocopherol and docetaxel presented synergistic cell growth inhibition and cell apoptosis induction effects in SKOV3 cells at a low dose, which suggesting that δ-tocopherol could improve the serious side effects of docetaxel.

scholarly journals Effect of 5-aza-2ˈ-deoxycytidine on p27Kip1, p21Cip1/Waf1/Sdi1, p57Kip2, and DNA methyltransferase 1 Genes Expression, Cell Growth Inhibition and Apoptosis Induction in Colon Cancer SW 480 and SW 948 Cell Lines

2020 ◽  
Vol 9 ◽  
pp. 1899
Author(s):  
Masumeh Sanaei ◽  
Fraidoon Kavoosi ◽  
Sedighe Nasiri
Keyword(s):  
Colon Cancer ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Line ◽  
Cell Lines ◽  
Dna Methyltransferase ◽  
Dna Methyltransferase 1 ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition ◽  
Genes Expression

Background: Dysregulation of the cell cycle has been reported in various cancers. Inactivation of the cyclin-dependent kinases inhibitors (CDKIs), CIP/KIP family, such as p21Cip1/Waf1/Sdi1, p27Kip1, and p57Kip2 genes because of hypermethylation has been shown in several cancers. Treatment with DNA demethylating agent 5-aza-2ˈ-deoxycytidine (5-Aza-CdR) has been indicated that affect genomic methylation and resulting in silenced genes reactivation in colon cancer. Previously, we evaluated the effect of 5-Aza-CdR on DNA methyltransferase 1 (DNMT1) gene expression in hepatocellular carcinoma (HCC) which encouraged us to design the current study. The present study aimed to evaluate the effect of 5-Aza-CdR on p21Cip1/Waf1/Sdi1, p27Kip1, p57Kip2, and DNAT1 genes expression, cell growth inhibition and apoptosis induction in colon cancer SW 480 and SW 948 cell lines. Materials and Methods: The effect of 5-aza-CdR on the SW 480 and SW 948 cells growth, apoptosis induction and genes expression were assessed by MTT assay, flow cytometry, and real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis respectively. Results: 5-aza-CdR inhibited cell growth as time- and dose-dependent manner significantly (P<0.001). The agent reactivated p15INK4, p16INK4, p18INK4, and p19INK4 genes expression and induced apoptosis at a concentration of 5 μM significantly. Besides, 5-aza-CdR had a more significant effect on the SW 480 cell line in comparison to SW 948 cell line. Conclusion: 5-Aza-CdR plays a key role in the up-regulation of p21Cip1/Waf1/Sdi1, p27Kip1, and p57Kip2 and down-regulation of DNMT1 genes resulting in cell growth inhibition and apoptosis induction. [GMJ.2020;9:e1899] DOI:10.31661/gmj.v9i0.1899

scholarly journals The Effect of a Retinoic Acid Derivative on Cell-Growth Inhibition in a Pulmonary Carcinoma Cell Line

2016 ◽  
Vol 39 (3) ◽  
pp. 308-312
Author(s):  
Tomomi Akita ◽  
Michiko Horiguchi ◽  
Chihiro Ozawa ◽  
Hiroshi Terada ◽  
Chikamasa Yamashita
Keyword(s):  
Retinoic Acid ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Line ◽  
Acid Derivative ◽  
Carcinoma Cell ◽  
Carcinoma Cell Line ◽  
Cell Growth Inhibition ◽  
Pulmonary Carcinoma

EFFECT OF VALPROIC ACID IN COMPARISON WITH VORINOSTAT ON CELL GROWTH INHIBITION AND APOPTOSIS INDUCTION IN THE HUMAN COLON CANCER SW48 CELLS IN VITRO

2018 ◽  
Vol 40 (2) ◽  
pp. 95-100 ◽  
Author(s):  
M Sanaei ◽  
F Kavoosi ◽  
O Mansoori
Keyword(s):  
Colon Cancer ◽  
Valproic Acid ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Histone Deacetylases ◽  
Regulation Of Gene Expression ◽  
Human Colon ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition ◽  
Human Colon Cancer

Aim: Acetylation levels of histones are the result of the balance between histone acetyltransfrases and histone deacetylases activities, which plays an important role in chromatin remodeling and regulation of gene expression. Histone deacetylases inhibitors such as valproic acid, vorinostat have attracted interest because of their ability to induce differentiation and apoptosis of cancer cells. The current study was designed to assess the effect of valproic acid in comparison to and in combination with vorinostat on cell growth inhibition and apoptosis induction in the human colon cancer SW48 cells. Materials and Methods: The colon cancer SW48 cells were seeded and treated with various doses of valproic acid and vorinostat and MTT assay and flow cytometric assay were done to determine cell viability and cell apoptosis, respectively. Results: All concentrations of both agents reduced viability significantly in a dose- and time-dependent fashion (p < 0.004). Both compounds, either single or combined agents, induced apoptosis significantly, whereas the ratio of the apoptotic cells treated with combined agents was more significant than the single. Conclusion: Our findings suggest that vaproic acid and vorinostat can significantly inhibit cell growth and induce apoptosis in colon cancer SW48 cells.

GDC-0449, the Small Molecule Inhibitor of Hedgehog-Gli Pathway for the Treatment of BCR-ABL Positive Leukemia Cells and In Combination with Dasatinib

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2136-2136
Author(s):  
Seiichi Okabe ◽  
Tetsuzo Tauchi ◽  
Kazuma Ohyashiki
Keyword(s):  
Cell Growth ◽  
Tyrosine Kinase ◽  
Growth Inhibition ◽  
Cell Line ◽  
Kinase Inhibitors ◽  
Leukemia Cells ◽  
Dependent Manner ◽  
Feeder Cell ◽  
Cell Growth Inhibition ◽  
Abl Tyrosine Kinase

Abstract Abstract 2136 Imatinib has shown clinical efficacy against Philadelphia chromosome (Ph) positive leukemia cells and it is now the standard care for initial therapy. However, recent studies reported imatinib are not effective in quiescent primitive chronic myeloid leukemia (CML) stem cells. Moreover, many Ph-positive leukemia patients develop resistance or fail to respond to imatinib by mutation in the ABL kinase domain in clinically. These results indicated that alternative combination therapy such as BCR-ABL targeting tyrosine kinase inhibitors (TKIs) and nontoxic agents are required to cure the Ph positive leukemia patients. Hedgehog (Hh)- Glioma-associated oncogene homolog (Gli) signaling regulates self-renewal of stem cells and implicates in a large number of human cancers. One of the Hh inhibitor, GDC-0449 is a potent small molecule inhibitor of Hedgehog-Gli pathway. It has been reported GDC-0449 showed high target specificity and demonstrated antiproliferative activity against tumors and it is now in clinical trial. Therefore, combination therapy using a BCR-ABL tyrosine kinase inhibitors and a Hedgehog-Gli inhibitor, GDC-0449 may help prevent CML relapse and these approaches may be expected to improve the outcomes of Ph-positive leukemia patients. In this study, we investigated the GDC-0449 efficacy by using the BCR-ABL positive cell lines, OM9;22, K562 and primary samples when leukemic cells were protected by the feeder cell line, S9 cells. We examined a comprehensive drug combination experiment using GDC-0449 and dual Src/ABL tyrosine kinase inhibitor, dasatinib. Gli proteins (Gli1, Gli2 and Gli3) were existed in Ph-positive cell lines. We found the cell numbers of OM9;22 were significantly increased with the feeder cell line, S9 cells compared to without S9 cells. The treatment of dasatinib exhibits cell growth inhibition partially against OM9;22 cells in the presence of feeder cell line, S9 cells. Caspase-3 activity by 100 nM dasatinib treatment was also reduced in the presence of S9 cells. 72 h of combined treatment of Ph-positive leukemia cells with 10 μM of GDC-0449 and 100 nM of dasatinib in the presence of feeder cell line, caused significantly more cytotoxicity than each drug alone. We next investigated the efficacy and intracellular signaling of GDC-0449. The treatment of GDC-0449 exhibits cell growth inhibition and induced apoptosis against OM9;22 cells in a dose and time dependent manner. Expression of Gli1 and Gli2 proteins were reduced after GDC-0449 treatment. 10 μM of GDC-0449 also inhibited the growth of Ph-positive primary samples by colony assay. Another Hh inhibitor, SANT-2 also exhibits cell growth inhibition against OM9;22 cells in a dose dependent manner. Data from this study suggested that administration of the Hh inhibitor, GDC-0449 may be a powerful strategy against Ph-positive leukemia cells and enhance cytotoxic effects of dasatinib in the presence of feeder cell. Disclosures: Ohyashiki: Nippon Shinyaku Co., Ltd.: Research Funding.

Effect of 5-fluoro-2′-deoxycytidine (FdCyd) on p16INK4a, p14ARF, p15INK4b, and DNA methyltransferase 1, 3a, and 3b Genes Expression, Apoptosis Induction, and Cell Growth Inhibition in Pancreatic Cancer AsPC-1 and Hepatocellular Carcinoma LCL-PI 11 Cell Li

2020 ◽  
Author(s):  
Masumeh Sanaei ◽  
Fraidoon Kavoosi
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Apoptosis ◽  
Dna Methyltransferase ◽  
Dna Methyltransferase 1 ◽  
Dependent Manner ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition ◽  
Genes Expression ◽  
Methyltransferase 1

Background: Aberrant DNA methylation of the promoter region is one of the most epigenetic changes in numerous cancers. DNA methyltransferase inhibitors (DNMTIs) can revert DNA hypermethylation in tumor suppressor genes (TSGs). The present study was designed to investigate the effect of 5-fluoro-2′-deoxycytidine (FdCyd) on p16INK4a, p14ARF, p15INK4b, and DNA methyltransferase 1, 3a, and 3b genes expression, apoptosis induction, cell growth inhibition in pancreatic cancer AsPC-1 and hepatocellular carcinoma LCL-PI 11 cell lines. Materials and Methods: The cells were treated with FdCyd at different periods. Then, the MTT assay, cell apoptosis assay, and qRT-PCR were done to determine cell viability, cell apoptosis, and the relative gene expression level respectively. Results: The FdCyd decreased DNA methyltransferase 1, 3a, and 3b and increased p16INK4a, p14ARF, and p15INK4b genes expression significantly (P<0.001). Besides, LCL-PI 11 cell was more sensitive to FdCyd in comparison to AsPC-1 cell. FdCyd induced significant cell growth inhibition with a dose- and time-dependent manner (P<0.001). The IC50 value of FdCyd was obtained with approximately 1μM. Further, FdCyd induced cell apoptosis significantly as a time-dependent manner. The number of apoptotic cells was significantly increased in all groups. The percentage of apoptotic cells after 24 and 48 h were 13.86 and 29.6 % in AsPC-1 and 21.04 and 41.52 % in LCL-PI 11 cell line respectively (P<0.001). Conclusion: The FdCyd can reactivate the p16INK4a, p14ARF, and p15INK4b through inhibition of DNA methyltransferase 1, 3a, and 3b gene expression.

scholarly journals The antitumor activity of 4,4′-bipyridinium amphiphiles

RSC Advances ◽  
2019 ◽  
Vol 9 (57) ◽  
pp. 33023-33028
Author(s):  
Senlin Wang ◽  
Hongshuai Wu ◽  
Fanghui Chen ◽  
Yu Zhang ◽  
Yuchen Zhang ◽  
...  
Keyword(s):  
Cell Growth ◽  
Antitumor Activity ◽  
Growth Inhibition ◽  
Apoptosis Induction ◽  
Cell Growth Inhibition

The cell growth inhibition and apoptosis induction of 4,4′-bipyridinium amphiphiles.

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