Activity of cyclin B1 in HL-60 cells treated with etoposide

Żuryń, Agnieszka; Krajewski, Adrian; Szulc, Dawid; Litwiniec, Anna; Grzanka, Alina

doi:10.1016/j.acthis.2016.05.010

Cited by 9 publications

(7 citation statements)

References 23 publications

(21 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, as indicated by their ability to prevent digestion of plasmid DNA with BamHI restriction nuclease, the studied chromanone/flavanone analogues appear to be capable of intercalating with genomic DNA of cancer cells, thus leading to cell damage and ultimately apoptosis. It is noteworthy that commercially-used anticancer drugs, such as docetaxel, doxorubicin, cisplatin or etoposide, are also known to arrest the cycle of cancer cells in the G2/M phase [32][33][34]. Our findings correspond closely with those of previous reports on the cell cycle distribution in HL-60 cells following treatment with cisplatin.…”

Section: Discussionsupporting

confidence: 91%

Biological Evaluation of 3-Benzylidenechromanones and Their Spiropyrazolines-Based Analogues

et al. 2020

View full text Add to dashboard Cite

A series of 3-benzylidenechrmanones 1, 3, 5, 7, 9 and their spiropyrazoline analogues 2, 4, 6, 8, 10 were synthesized. X-ray analysis confirms that compounds 2 and 8 crystallize in a monoclinic system in P21/n space groups with one and three molecules in each asymmetric unit. The crystal lattice of the analyzed compounds is enhanced by hydrogen bonds. The primary aim of the study was to evaluate the anti-proliferative potential of 3-benzylidenechromanones and their spiropyrazoline analogues towards four cancer cell lines. Our results indicate that parent compounds 1 and 9 with a phenyl ring at C2 have lower cytotoxic activity against cancer cell lines than their spiropyrazolines analogues. Analysis of IC50 values showed that the compounds 3 and 7 exhibited higher cytotoxic activity against cancer cells, being more active than the reference compound (4-chromanone or quercetin). The results of this study indicate that the incorporation of a pyrazoline ring into the 3-arylideneflavanone results in an improvement of the compounds’ activity and therefore it may be of use in the search of new anticancer agents. Further analysis allowed us to demonstrate the compounds to have a strong inhibitory effect on the cell cycle. For instance, compounds 2, 10 induced 60% of HL-60 cells to be arrested in G2/M phase. Using a DNA-cleavage protection assay we also demonstrated that tested compounds interact with DNA. All compounds at the concentrations corresponding to cytotoxic properties are not toxic towards red blood cells, and do not contribute to hemolysis of RBCs.

show abstract

Section: Discussionsupporting

confidence: 91%

Biological Evaluation of 3-Benzylidenechromanones and Their Spiropyrazolines-Based Analogues

et al. 2020

View full text Add to dashboard Cite

show abstract

“…6). Our results are in agreement with data obtained by Żuryń and colleagues on HL-60 cells treated with 0.5-1 µM etoposide 21 . We also observed a slight decrease in the number of S phase cells after incubation with etoposide (p < 0.05)20.…”

Section: Resultssupporting

confidence: 94%

Kaempferol and Its Glycoside Derivatives as Modulators of Etoposide Activity in HL-60 Cells

Kluska

Juszczak

Żuchowski

et al. 2021

Preprint

View full text Add to dashboard Cite

Kaempferol is a polyphenol found in a variety of plants. Kaempferol has antitumor properties by affecting proliferation and apoptosis of cancer cells. We investigated whether kaempferol and its glycoside derivatives: kaempferol 3-O-[(6-O-E-caffeoyl)-β-D-glucopyranosyl-(1→2)]-β-D-galactopyranoside-7-O-β-D -glucuropyranoside (P2), kaempferol 3-O-[(6-O-E-p-coumaroyl)-β-D-glucopyranosyl-(1→2)]-β-D-galactopyranoside-7-O-β-D-glucuropyranoside (P5) and kaempferol 3-O-[(6-O-E-feruloyl)-β-D-glucopyranosyl-(1→2)]-β-D-galactopyranoside-7-O-β-D-glucuropyranoside (P7) isolated from aerial parts of Lens culinaris Medik. affect the antitumor activity of etoposide in HL-60 cells. We analyzed the effect of kaempferol and its derivatives on cytotoxicity, DNA damage, apoptosis, cell cycle progression and free radicals induced by etoposide. We also studied the impact of kaempferol and its derivatives on the expression of HO-1 and Nrf-2 genes in HL-60 cells. We demonstrated that kaempferol increases the sensitivity of HL-60 cells to etoposide but does not affect apoptosis induced by this drug. Kaempferol also reduces the level of free radicals generated by etoposide. Unlike kaempferol, some of its derivatives reduce the apoptosis of HL-60 cells (P2 and P7) and increase the level of free radicals (P2 and P5) induced by etoposide. Our results indicate that kaempferol derivatives may have an opposite effect on the action of etoposide in HL-60 cells compared to kaempferol.

show abstract

“…To further understand the molecular mechanism of highly expressed KIF18A in HCC, we detected the expression of some proteins that are associated with cancer-related signal pathways by western blot, including cell cycle-related protein (cyclin B1), oncogene Akt, and metastasis-associated proteins (MMP-7, MMP-9). Cyclin B1 regulates mitosis in the G2/M phase of the cell cycle, and abnormalities in cyclin B1 may cause tumorigenesis [ 17 , 18 ]. MMP-7 and MMP-9 are the main proteases of zinc-dependent endopeptidases and participate in extracellular matrix degradation, which is associated with the movement of tumour cells [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

The role of kinesin KIF18A in the invasion and metastasis of hepatocellular carcinoma

Luo

Liao

et al. 2018

World J Surg Onc

View full text Add to dashboard Cite

BackgroundKIF18A is associated with a variety of tumours; however, the specific mechanism of action of KIF18A in hepatocellular carcinoma (HCC) remains unclear. In this study, in vitro and in vivo experiments were performed with the aim of exploring the potential function and molecular mechanism of kinesin KIF18A in the occurrence and development of HCC.MethodsWe detected the expression of KIF18A in tumour and adjacent tissues as well as cell proliferation, cell invasion and migration in hepatoma cells after silencing KIF18A. KIF18A-silenced hepatoma cells were subcutaneously injected into nude mice to verify the tumorigenicity of KIF18A. We also detected the expression of signal pathway-related proteins in hepatoma cells after KIF18A knockdown with the aim of exploring the association between KIF18A and related signalling pathways.ResultsThe level of KIF18A protein was higher in liver cancer tissues than adjacent tissues. After silencing KIF18A in SMMC-7721 and HepG2 cells, cell growth was obviously inhibited; the migration and invasion abilities were significantly decreased and the in vivo tumour weight was decreased compared to the control group (0.201 ± 0.088 g vs 0.476 ± 0.126 g, p = 0.009). The expression of cell cycle-related protein (cyclin B1), invasion and metastasis-related proteins (MMP-7 and MMP-9) and Akt-related proteins in hepatoma cells was also decreased after knocking down KIF18A.ConclusionsKIF18A may promote proliferation, invasion and metastasis of HCC cells by promoting the cell cycle signalling pathway as well as the Akt and MMP-7/MMP-9-related signalling pathways and may serve as a new target for the diagnosis and treatment of HCC.

show abstract

Activity of cyclin B1 in HL-60 cells treated with etoposide

Cited by 9 publications

References 23 publications

Biological Evaluation of 3-Benzylidenechromanones and Their Spiropyrazolines-Based Analogues

Biological Evaluation of 3-Benzylidenechromanones and Their Spiropyrazolines-Based Analogues

Kaempferol and Its Glycoside Derivatives as Modulators of Etoposide Activity in HL-60 Cells

The role of kinesin KIF18A in the invasion and metastasis of hepatocellular carcinoma

Contact Info

Product

Resources

About