scholarly journals Extract of Juniperus indica Bertol Synergizes with Cisplatin to Inhibit Oral Cancer Cell Growth via Repression of Cell Cycle Progression and Activation of the Caspase Cascade

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2746 ◽  
Author(s):  
Xiao-Fan Huang ◽  
Kai-Fu Chang ◽  
Shan-Chih Lee ◽  
Chia-Yu Li ◽  
Hung-Hsiu Liao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Oral Cancer ◽  
Anticancer Agents ◽  
Cell Cycle Progression ◽  
Anticancer Agent ◽  
Synergistic Effects ◽  
Cancer Cell Growth ◽  
Cycle Progression ◽  
Common Cancer ◽  
Caspase Cascade

Oral cancer—a type of head and neck cancer—is estimated to be the fifth most common cancer in Taiwan. However, efficacious therapies for oral cancer are still lacking due to drug resistance and recurrence. Consequently, the identification of new anticancer agents for clinical treatment is needed. Juniperus indica Bertol is a plant of the Juniperus genus often used as a treatment in traditional medicine due to its anti-inflammatory, antibacterial and diuretic functions. The biofunctions of Juniperus indica Bertol including its anticancer potential, have not been fully explored. As a result, the aim of this research was to investigate the anticancer activity of Juniperus indica Bertol extract (JIB extract) and determine whether JIB extract has synergistic effects with cisplatin in oral cancer. These results are the first to demonstrate that JIB extract exhibits anticancer capacity and synergizes with cisplatin to treat oral cancer. Our findings indicate that JIB extract has a potential to develop anticancer agent and chemo therapeutic adjuvant for oral cancer.

scholarly journals A bulky glycocalyx fosters metastasis formation by promoting G1 cell cycle progression

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Elliot C Woods ◽  
FuiBoon Kai ◽  
J Matthew Barnes ◽  
Kayvon Pedram ◽  
Michael W Pickup ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Cells ◽  
Cell Cycle Progression ◽  
Disseminated Tumor Cells ◽  
Metastatic Potential ◽  
Cancer Cell Growth ◽  
Cycle Progression ◽  
Growth And Survival ◽  
Syngeneic Mouse Model

Metastasis depends upon cancer cell growth and survival within the metastatic niche. Tumors which remodel their glycocalyces, by overexpressing bulky glycoproteins like mucins, exhibit a higher predisposition to metastasize, but the role of mucins in oncogenesis remains poorly understood. Here we report that a bulky glycocalyx promotes the expansion of disseminated tumor cells in vivo by fostering integrin adhesion assembly to permit G1 cell cycle progression. We engineered tumor cells to display glycocalyces of various thicknesses by coating them with synthetic mucin-mimetic glycopolymers. Cells adorned with longer glycopolymers showed increased metastatic potential, enhanced cell cycle progression, and greater levels of integrin-FAK mechanosignaling and Akt signaling in a syngeneic mouse model of metastasis. These effects were mirrored by expression of the ectodomain of cancer-associated mucin MUC1. These findings functionally link mucinous proteins with tumor aggression, and offer a new view of the cancer glycocalyx as a major driver of disease progression.

scholarly journals XRCC2 Promotes Colorectal Cancer Cell Growth, Regulates Cell Cycle Progression, and Apoptosis

Medicine ◽  
2014 ◽  
Vol 93 (28) ◽  
pp. e294 ◽  
Author(s):  
Kaiwu Xu ◽  
Xinming Song ◽  
Zhihui Chen ◽  
Changjiang Qin ◽  
Yulong He ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Colorectal Cancer Cell ◽  
Cancer Cell Growth ◽  
Cycle Progression

scholarly journals Ethanol, Zn2+ and insulin interact as progression factors to enhance DNA synthesis synergistically in the presence of Ca2+ and other cell cycle initiators in fibroblasts

2000 ◽  
Vol 346 (1) ◽  
pp. 241-247 ◽  
Author(s):  
Jin-Sheng HUANG ◽  
Qing-Bai SHE ◽  
Karan S. CRILLY ◽  
Zoltan KISS
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Dna Synthesis ◽  
Cell Cycle Progression ◽  
Synergistic Effects ◽  
Dependent Manner ◽  
Cycle Progression ◽  
3T3 Fibroblasts ◽  
Igf I ◽  
Nih 3T3

In serum-starved NIH 3T3 fibroblasts, ethanol (30-80 mM) promoted the effects of insulin and insulin-like growth factor I (IGF-I) on DNA synthesis in a Zn2+-dependent manner. Ethanol and Zn2+ were most effective when added shortly before or after insulin, indicating that all these agents facilitated cell cycle progression. The synergistic effects of ethanol, Zn2+ and insulin (or IGF-I) on DNA synthesis required 1.1-2.3 mM Ca2+, which seemed to act as the cell cycle initiator. When serum-starved cells were pretreated for 2 h with other cell cycle initiators such as 10% (v/v) serum, 50 ng/ml platelet-derived growth factor or 2 ng/ml fibroblast growth factor, subsequent co-treatments with 60 mM ethanol, Zn2+ and insulin for an 18 h period again synergistically increased DNA synthesis. Of the various signal transducing events examined, ethanol stimulated cellular uptake of 45Ca and it enhanced the stimulatory effects of insulin on p70 S6 kinase activity in a Zn2+-dependent manner. In contrast, ethanol inhibited insulin-induced activating phosphorylation of p42/p44 mitogen-activated protein kinases; these inhibitory ethanol effects were prevented by Zn2+. The results show that, in NIH 3T3 fibroblasts, ethanol can promote cell cycle progression in the presence of a cell cycle initiator as well as Zn2+ and insulin (or IGF-I).

scholarly journals Identification and Validation of Potential Candidate Genes of Colorectal Cancer in Response to Fusobacterium nucleatum Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiangguo Zhang ◽  
Zhimo Wang ◽  
Hong Lv ◽  
Guojun Li
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Candidate Genes ◽  
Cell Cycle Progression ◽  
Cell Model ◽  
Fusobacterium Nucleatum ◽  
Potential Candidate ◽  
Cancer Cell Growth ◽  
Cycle Progression ◽  
The Relationship

Objective: Recent investigations revealed the relationship between Fusobacterium nucleatum (Fn) infection and colorectal cancer (CRC). However, how the host genes changes contribute to CRC in response to Fn infection remains largely unknown.Materials and methods: In the present study, we aimed to comprehensively analyze microarray data obtained from a Caco-2 infection cell model using integrated bioinformatics analysis and further identify and validate potential candidate genes in Fn-infected Caco-2 cells and CRC specimens.Results: We identified 10 hub genes potentially involved in Fn induced tumor initiation and progression. Furthermore, we demonstrated that the expression of centrosomal protein of 55 kDa (CEP55) is significantly higher in Fn-infected Caco-2 cells. Knocking down of CEP55 could arrest the cell cycle progression and induce apoptosis in Fn-infected Caco-2 cells. The expression of CEP55 was positively correlated with the Fn amount in Fn-infected CRC patients, and these patients with high CEP55expression had an obviously poorer differentiation, worse metastasis and decreased cumulative survival rate.Conclusion: CEP55 plays an important role in Fn-infected colon cancer cell growth and cell cycle progression and could be used as a new diagnostic and prognostic biomarker for Fn-infected CRC.

Natural sourced inhibitors of EGFR, PDGFR, FGFR and VEGFR-mediated signaling pathways as potential anticancer agents

2021 ◽  
Vol 28 ◽  
Author(s):  
Sisir Nandi ◽  
Rishita Dey ◽  
Asmita Samadder ◽  
Aaruni Saxena ◽  
Anil Kumar Saxena
Keyword(s):  
Cell Cycle ◽  
Cancer Progression ◽  
Anticancer Agents ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Mitotic Cell ◽  
Cell Cycle Checkpoints ◽  
Signalling Pathways ◽  
Mitotic Cell Cycle ◽  
Cycle Progression

: The molecular mechanisms of mitotic cell cycle progression involve very tightly restricted types of machinery which are highly regulated by a fine balance between the positive and negative accelerators (or regulators). These regulators include several checkpoints that have proteins acting as enzymes and their activating partners. These checkpoints incessantly monitor the external as well as internal environments such as growth signals, favorable conditions for growth, cell size, DNA integrity of the cell and hence function to maintain the highly ordered cell cycle progression by sustaining cell homeostasis and promotes error-free DNA replication and cell cycle, division. To progress through the mitotic cell cycle, the cell has to successfully drive past the cell cycle checkpoints. Due to the abnormal behavior of some cell cycle proteins, the cells tend to divide continuously overcoming the tight regulation of cell cycle checkpoints. Such anomalies may lead to unwanted cell division and this deregulation of cell cycle events is considered as one of the main reasons behind tumor development and thus cancer progression. So the understanding of the molecular mechanisms in cancer progression might be insightful for designing several cancer treatment strategies. The deregulation in the checkpoints is caused due to the changes brought in the tyrosine residues of TPKs via PDGFR, EGFR, FGFR, and VEGFR-mediated signalling pathways. Therefore, the inhibitors of PDGFR, EGFR, FGFR, and VEGFR-mediated signalling pathways would be potential anticancer agents. The resistance and toxicity in the existing synthetic anticancer chemotherapeutics may decrease the life span of a patient. For a long, natural products have always played an essential alternative source of therapeutic agents due to having the least or no side effect and toxicity. The present study is an attempt to promote the natural anticancer drug development focusing on the updated structural information of PDGFR, EGFR, FGFR, and VEGFR inhibitors isolated from the plant sources. The data used in this review has been collected from internet resources viz. GOOGLE Web, GOOGLE SCHOLAR, and PubMed Central. The citation of each report was first checked after which the articles were selected as an authentic reference for the present study. Around 200 journal articles were selected of which around 142 were selected finally for presenting the study on the natural sourced inhibitors of EGFR, PDGFR, FGFR, and VEGFR-mediated signaling pathways which would help in the potential cancer treatment.

scholarly journals Capsaicin Targets tNOX (ENOX2) to Inhibit G1 Cyclin/CDK Complex, as Assessed by the Cellular Thermal Shift Assay (CETSA)

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1275 ◽  
Author(s):  
Atikul Islam ◽  
Ally J. Su ◽  
Zih-Ming Zeng ◽  
Pin Ju Chueh ◽  
Ming-Hung Lin
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Nadh Oxidase ◽  
Cancer Cell Growth ◽  
Cycle Progression ◽  
Thermal Shift Assay ◽  
G1 Cyclin ◽  
Cellular Thermal Shift Assay ◽  
Thermal Shift

Capsaicin (8-methyl-N-vanillyl-6-noneamide), which is an active component in red chili peppers, is used as a chemopreventive agent that shows favorable cytotoxicity against cancer cells. Accumulating evidence indicates that capsaicin preferentially inhibits a tumor-associated NADH oxidase (tNOX, ENOX2) that is ubiquitously expressed in cancer but not in non-transformed cells. This attenuates cancer cell growth by inducing apoptosis. The capsaicin-mediated inhibition of tNOX was recently shown to prolong the cell cycle. However, the molecular events underlying this regulation have not yet been investigated. In the present study, we used a cellular thermal shift assay (CETSA) to detect “target engagement” of capsaicin and its consequent impact on cell cycle progression. Our results indicated that capsaicin engaged with tNOX and triggered the proteasomal degradation of tNOX, which leads to the inhibition of NAD+-dependent SIRT1 deacetylase. Ultimately, the acetylation levels of c-Myc and p53 were enhanced, which suppressed the activation of G1 cyclin/Cyclin-dependent kinase complexes and triggered cell cycle arrest in cancer cells. The results obtained when tNOX was overexpressed in non-cancer cells validated its importance in cell cycle progression. These findings provide the first molecular insights into the regulatory role of tNOX and the anti-proliferative property of capsaicin in regulating the cell cycle of bladder cancer cells.

scholarly journals Chrysophanol Regulates Cell Death, Metastasis, and Reactive Oxygen Species Production in Oral Cancer Cell Lines

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Po-Chih Hsu ◽  
Ching-Feng Cheng ◽  
Po-Chun Hsieh ◽  
Yi-Hsuan Chen ◽  
Chan-Yen Kuo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Cell Death ◽  
Oral Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cycle Progression

Background. Oral cancer belongs to the class of head and neck cancers and can be life threatening if not diagnosed and treated early. Activation of cell death via apoptosis or reactive oxygen species (ROS) accumulation and inhibition of cell cycle progression, migration, and epithelial-to-mesenchymal transition (EMT) may be a good strategy to arrest the development of oral cancer. In this study, we analyzed the possible action of chrysophanol isolated from the rhizomes of Rheum palmatum on the oral cancer cell lines FaDu (human pharynx squamous cell carcinoma) and SAS (human tongue squamous carcinoma) by investigating whether chrysophanol could influence cell death. Method. Cell viability was measured by using the MTT assay. For the detection of apoptosis, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and subG1 population analysis were used. We also examined cell cycle progression and ROS levels by flow cytometry. Additionally, the expression of p53, p21, procaspase 3, cyclin D1, CDK4, cdc2, CDK2, E-cadherin, vimentin, and PCNA was evaluated by western blotting. Conclusion. Chrysophanol has an anticancer effect on FaDu and SAS cell lines. There is an increase in subG1 accumulation, ROS production, and cell cycle G1 arrest after treatment with chrysophanol. On the other hand, chrysophanol inhibited cell migration/metastasis and EMT. We proposed that chrysophanol may be a good candidate compound on oral cancer treatment in the further.

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