scholarly journals Cattleianal and Cattleianone: Two New Meroterpenoids from Psidium cattleianum Leaves and Their Selective Antiproliferative Action against Human Carcinoma Cells

Molecules ◽  
2021 ◽  
Vol 26 (10) ◽  
pp. 2891
Author(s):  
Engy A. Mahrous ◽  
Ahmed M. Al-Abd ◽  
Maha M. Salama ◽  
Magda M. Fathy ◽  
Fathy M. Soliman ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Annexin V ◽  
Carcinoma Cells ◽  
Cell Cycle Analysis ◽  
Breast Adenocarcinoma ◽  
Human Carcinoma ◽  
Psidium Cattleianum ◽  
Antiproliferative Action ◽  
Adenocarcinoma Cells ◽  
Ht 29

The Myrteacae family is known as a rich source of phloroglucinols, a group of secondary metabolites with notable biological activities. Leaves of Psidium cattleianum were extracted with chloroform: methanol 8:2 to target the isolation of phloroglucinol derivatives. Isolated compounds were characterized using different spectroscopic methods: nuclear magnetic resonance (NMR), ultra-violet (UV) and mass spectrometry (MS). Two new phloroglucinols were evaluated for cytotoxicity against a panel of six human cancer cell lines, namely colorectal adenocarcinoma cells (HT-29 and HCT-116); hepatocellular carcinoma cells (HepG-2); laryngeal carcinoma (Hep-2); breast adenocarcinoma cells (MCF7 and MDA-MB231), in addition to normal human melanocytes HFB-4. Additionally, cell cycle analysis and annexin-V/FITC-staining were used to gain insights into the mechanism of action of the isolated compounds. The new phloroglucinol meroterpenoids, designated cattleianal and cattleianone, showed selective antiproliferative action against HT-29 cells with IC50’s of 35.2 and 32.1 μM, respectively. Results obtained using cell cycle analysis and annexin-V/FITC-staining implicated both necrosis and apoptosis pathways in the selective cytotoxicity of cattleianal and cattleianone. Our findings suggest that both compounds are selective antiproliferative agents and support further mechanistic studies for phloroglucinol meroterpenoids as scaffolds for developing new selective chemotherapeutic agents.

scholarly journals Cytotoxic Effects of Cannabinoids on Human HT-29 Colorectal Adenocarcinoma Cells: Different Mechanisms of THC, CBD, and CB83

2020 ◽  
Vol 21 (15) ◽  
pp. 5533 ◽  
Author(s):  
Daniela Cerretani ◽  
Giulia Collodel ◽  
Antonella Brizzi ◽  
Anna Ida Fiaschi ◽  
Andrea Menchiari ◽  
...  
Keyword(s):  
Colorectal Carcinoma ◽  
Cell Viability ◽  
Annexin V ◽  
Ascorbic Acid Content ◽  
Carcinoma Cells ◽  
Cytotoxic Effects ◽  
Adenocarcinoma Cells ◽  
Malondialdehyde Content ◽  
Ht 29 ◽  
In Cells

In this study, we investigated the effects of exposition to IC50 dose for 24 h of a new synthetic cannabinoid (CB83) and of phytocannabinoids Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) on HT-29 colorectal carcinoma cells. Cell viability and proliferative activity evaluated using the MTT, lactate dehydrogenase (LDH), and CyQUANT assays showed that cell viability was significantly affected when CB83, THC, and CBD were administered to cells. The results obtained showed that the reduced glutathione/oxidized glutathione ratio was significantly reduced in the cells exposed to CBD and significantly increased in the cells treated with the CB83 when compared to the controls. CBD treatment causes a significant increase in malondialdehyde content. The catalase activity was significantly reduced in HT-29 cells after incubation with CB83, THC, and CBD. The activities of glutathione reductase and glutathione peroxidase were significantly increased in cells exposed to THC and significantly decreased in those treated with CBD. The ascorbic acid content was significantly reduced in cells exposed to CB83, THC, and CBD. The ultrastructural investigation by TEM highlighted a significantly increased percentage of cells apoptotic and necrotic after CB83 exposition. The Annexin V-Propidium Iodide assay showed a significantly increased percentage of cells apoptotic after CB83 exposition and necrotic cells after CBD and THC exposition. Our results proved that only CBD induced oxidative stress in HT-29 colorectal carcinoma cells via CB receptor-independent mechanisms and that CB83 caused a mainly CB2 receptor-mediated antiproliferative effect comparable to 5-Fuorouracil, which is still the mainstay drug in protocols for colorectal cancer.

scholarly journals LAMA-1: A Cerebroside Isolated from the Deep-Sea-Derived Fungus Penicillium chrysogenum

Metabolites ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 75
Author(s):  
Samah O. Alshehri ◽  
Rania T. Malatani ◽  
Hanin A. Bogari ◽  
Ahmad O. Noor ◽  
Amany K. Ibrahim ◽  
...  
Keyword(s):  
Cell Lines ◽  
Penicillium Chrysogenum ◽  
2D Nmr ◽  
Carcinoma Cells ◽  
Breast Adenocarcinoma ◽  
Cytotoxic Activities ◽  
Human Carcinoma ◽  
Sulforhodamine B ◽  
Ic50 Values ◽  
Hepg2 Cell Lines

Chemical investigation of the ethyl acetate extract of Penicillium chrysogenum strain S003, a fungus isolated from Red Sea deep sediment, led to the isolation of a cerebroside molecular species LAMA (1) along with three other known compounds, ergosterol (2), epidioxyergosterol (3), and kojic acid (4). The structures of the isolated compounds were elucidated by interpretation of spectral data, including detailed 1D and 2D NMR (One and two dimensional Nuclear Magnetic Resonance) and mass spectrometry. The cytotoxic activities of isolated compounds 1–4 against five human carcinoma cells were evaluated using sulforhodamine B (SRB) assay. Compounds 2 and 3 displayed promising cytotoxic profiles against lung cancer (A-549), prostate (DU-145), breast adenocarcinoma (MCF-7), and hepatocellular (HepG2) cell lines, with IC50 values of 21.26, 19.3; 1.50, 6.10; 16.95, 13.6; and 2.89, 3.07 µM, respectively, while they were inactive against HeLa cells. Compounds 1 and 4 showed weak cytotoxic profiles against all cell lines under investigation.

scholarly journals Rapid on-chip apoptosis assay on human carcinoma cells based on annexin-V/quantum dot probes

2017 ◽  
Vol 94 ◽  
pp. 408-414 ◽  
Author(s):  
Helena Montón ◽  
Mariana Medina-Sánchez ◽  
Joan Antoni Soler ◽  
Andrzej Chałupniak ◽  
Carme Nogués ◽  
...  
Keyword(s):  
Quantum Dot ◽  
Annexin V ◽  
Carcinoma Cells ◽  
Human Carcinoma ◽  
Apoptosis Assay ◽  
On Chip

scholarly journals AP-2γ Induces p21 Expression, Arrests Cell Cycle, Inhibits the Tumor Growth of Human Carcinoma Cells

Neoplasia ◽  
2006 ◽  
Vol 8 (7) ◽  
pp. 568-577 ◽  
Author(s):  
Hualei Li ◽  
Prabhat C. Goswami ◽  
Frederick E. Domann
Keyword(s):  
Cell Cycle ◽  
Tumor Growth ◽  
Carcinoma Cells ◽  
Human Carcinoma

scholarly journals Src activity increases and Yes activity decreases during mitosis of human colon carcinoma cells.

1995 ◽  
Vol 15 (5) ◽  
pp. 2374-2382 ◽  
Author(s):  
J Park ◽  
C A Cartwright
Keyword(s):  
Cell Cycle ◽  
Colon Carcinoma ◽  
Human Colon ◽  
T Antigen ◽  
Carcinoma Cells ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma ◽  
Polyomavirus Middle T Antigen ◽  
Middle T Antigen ◽  
Ht 29

Src and Yes protein-tyrosine kinase activities are elevated in malignant and premalignant tumors of the colon. To determine whether Src activity is elevated throughout the human colon carcinoma cell cycle as it is in polyomavirus middle T antigen- or F527 Src-transformed cells, and whether Yes activity, which is lower than that of Src in the carcinoma cells, is regulated differently, we measured their activities in cycling cells. We observed that the activities of both kinases were higher throughout all phases of the HT-29 colon carcinoma cell cycle than in corresponding phases of the fibroblast cycle. In addition, during mitosis of HT-29 cells, Src specific activity increased two- to threefold more, while Yes activity and abundance decreased threefold. The decreased steady-state protein levels of Yes during mitosis appeared to be due to both decreased synthesis and increased degradation of the protein. Inhibition of tyrosine but not serine/threonine phosphatases abolished the mitotic activation of Src. Mitotic Src was phosphorylated at novel serine and threonine sites and dephosphorylated at Tyr-527. Two cellular proteins (p160 and p180) were phosphorylated on tyrosine only during mitosis. Tyrosine phosphorylation of several other proteins decreased during mitosis. Thus, Src in HT-29 colon carcinoma cells, similar to Src complexed to polyomavirus middle T antigen or activated by mutation at Tyr-527, is highly active in all phases of the cell cycle. Moreover, Src activity further increases during mitosis, whereas Yes activity and abundance decrease. Thus, Src and Yes appear to be regulated differently during mitosis of HT-29 colon carcinoma cells.

scholarly journals Bcl-2 activates a programme of premature senescence in human carcinoma cells

2003 ◽  
Vol 375 (2) ◽  
pp. 263-274 ◽  
Author(s):  
Elvira CRESCENZI ◽  
Giuseppe PALUMBO ◽  
Hugh J. M. BRADY
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Cycle Progression ◽  
Constitutive Expression ◽  
Carcinoma Cells ◽  
Quiescent State ◽  
Premature Senescence ◽  
Human Carcinoma ◽  
Morphological Alterations ◽  
Cycle Arrest

The apoptosis regulator Bcl-2 has been shown to modulate cell-cycle progression, favouring a quiescent state over a proliferative state, in both normal and tumour cells. We show here that constitutive expression of Bcl-2 in human carcinoma cells results in a cell-cycle arrest that within a few days can become irreversible. Arrested cells acquire a senescent-like phenotype, which consists of several characteristic morphological alterations and increased activity of senescence-associated β-galactosidase. The induction of the premature senescence programme is mediated by inhibition of Cdk2 kinase activity, and p27KIP1 is required to maintain the senescent phenotype. We propose that the ability to activate an endogenous premature senescence programme allows Bcl-2 to suppress tumour growth. These results suggest that the down-regulation of Bcl-2 expression, which has been observed during the development and progression of human carcinoma, is related to the ability of Bcl-2 to severely hamper the growth of carcinoma cells and to induce a permanent cell-cycle arrest, with the features of senescence.

scholarly journals Mechanisms of Colorectal Cancer Cell Growth and Metastasis Inhibition By Carp-1 Functional Mimetic-4

2020 ◽  
Vol 18 (2) ◽  
Author(s):  
Abdelkader E. Ashour ◽  
Anwar A. Almuslim ◽  
Ashok Kumar ◽  
Khairy M. A. Zoheir ◽  
Rehan Ahmed ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Annexin V ◽  
Negative Regulator ◽  
Cell Cycle Analysis ◽  
High Recurrence Rate ◽  
Caspase 8 ◽  
Cancer Cell Growth ◽  
Qrt Pcr

Introduction: Colorectal cancer (CRC) constitutes one of the most aggressive malignancies worldwide and in Malaysia. Due to high recurrence rate and toxic side effects associated with radiation and chemotherapies, new agents are urgently needed. CARP-1 is a peri-nuclear phospho-protein which plays a dynamic role in regulating cell growth and apoptosis. CARP-1 functional mimetics (CFMs) are a class of compounds that stimulate CARP-1. CFM-4, a lead compound, was shown to suppress growth and metastasis of various cancers, other than CRC. We hypothesized that CFM-4 inhibits proliferation and metastasis in CRC. Materials and method:  CFM-4 anti-cancer effects of on CRC cells were investigated using MTT assay, Annexin V/Propidium iodide (PI) apoptosis assay, cell cycle analysis, quantitative real-time PCR (qRT-PCR) and Western blotting. Antimetastatic activities were assessed by migration, colony formation and invasion assays. Results: CFM-4 inhibited CRC cell proliferation and was much more potent than the classical anti-CRC 5-fluorouracil. These effects were shown to be mediated at least in part by stimulating apoptosis, as indicated in our Annexin V/PI assay results. Cell cycle analysis showed that CFM-4 induced G2/M phase arrest. Molecularly, qRT-PCR results revealed that CFM-4 promoted intrinsic apoptosis by upregulating expression of  caspase-8  and  -9 ,  p53,   PUMA  and  Noxa,  and stimulated extrinsic apoptosis by enhancing expression of death receptors (DR4 and DR5). CFM-4 upregulated  NF- k B  signaling inhibitor A20-binding inhibitor protein and the  PI3K  negative regulator  PTEN.  Western blot analysis results revealed that CFM-4 enhanced expression of CARP1, caspase-8 and executioner caspase-3. Metastatic properties of the CRC cells were reduced by CFM-4 through blocking their capabilities to form colonies, migrate and invade through the matrix-coated membranes. Conclusion: The potent antitumor and anti-metastatic properties of CFM-4 against CRC are due to collective pro-apoptotic, anti-proliferative and anti-metastatic activities. Together our data warrants further investigations of CFM-4 as potential anti-tumor agent for CRC malignancy and metastasis.

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