Cancer Cell Growth in the Near Infrared Region by Using Silica Coated Gold Nanorods

NANO ◽  
2020 ◽  
Vol 15 (01) ◽  
pp. 2050001 ◽  
Author(s):  
Tuntun Wang ◽  
Kwi Seok Yeom ◽  
Sitansu Sekhar Nanda ◽  
Seong Soo A. An ◽  
Dong Kee Yi
Keyword(s):  
Protein Folding ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gold Nanorods ◽  
Near Infrared ◽  
Infrared Region ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Cell Behaviors

Gold nanorods (AuNRs) have been considered as suitable materials for diverse biomedical applications in controlling cell behaviors. The nanoisland system with well-dispersed silica coated Au nanorods (Si-AuNRs) was used to demonstrate the enhanced cell growth of normal and cancer cells (MDA-MB-231 mammalian breast cancer cells) from the induced expressions of the heat shock proteins (HSPs). The over-expressions of HSP could help in protein folding in cell proliferations and growths of both the normal and cancer cells. In the current study, interesting mechanisms of cancer cell growth with Si-AuNRs than the conventional systems, such as incubator, would be presented. We believe that the growth of cancer cells in near infrared (NIR) region using Si-AuNRs induced the activities of HSPs, which could help the protein folding in cell growth and survival in comparison to the cells grown in the incubator only. The cell growth enhancing technology could be expanded in diverse applications in cell culture systems.

scholarly journals Starve Cancer Cells of Glutamine: Break the Spell or Make a Hungry Monster?

Cancers ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 804 ◽  
Author(s):  
Jie Jiang ◽  
Sankalp Srivastava ◽  
Ji Zhang
Keyword(s):  
Amino Acid ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Therapeutic Strategy ◽  
Glutamine Metabolism ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Tumor Environment ◽  
Cell Growth And Survival

Distinct from normal differentiated tissues, cancer cells reprogram nutrient uptake and utilization to accommodate their elevated demands for biosynthesis and energy production. A hallmark of these types of reprogramming is the increased utilization of, and dependency on glutamine, a nonessential amino acid, for cancer cell growth and survival. It is well-accepted that glutamine is a versatile biosynthetic substrate in cancer cells beyond its role as a proteinogenic amino acid. In addition, accumulating evidence suggests that glutamine metabolism is regulated by many factors, including tumor origin, oncogene/tumor suppressor status, epigenetic alternations and tumor microenvironment. However, despite the emerging understanding of why cancer cells depend on glutamine for growth and survival, the contribution of glutamine metabolism to tumor progression under physiological conditions is still under investigation, partially because the level of glutamine in the tumor environment is often found low. Since targeting glutamine acquisition and utilization has been proposed to be a new therapeutic strategy in cancer, it is central to understand how tumor cells respond and adapt to glutamine starvation for optimized therapeutic intervention. In this review, we first summarize the diverse usage of glutamine to support cancer cell growth and survival, and then focus our discussion on the influence of other nutrients on cancer cell adaptation to glutamine starvation as well as its implication in cancer therapy.

Cancer-associated fibroblasts (CAFs) in thyroid papillary carcinoma: molecular networks and interactions

2021 ◽  
pp. jclinpath-2020-207357
Author(s):  
Jeehoon Ham ◽  
Bin Wang ◽  
Joseph William Po ◽  
Amandeep Singh ◽  
Navin Niles ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Stromal Cells ◽  
Cancer Metastasis ◽  
Current Knowledge ◽  
Molecular Networks ◽  
Cancer Cell Growth ◽  
Molecular Events

In 1989, Stephen Paget proposed the ‘seed and soil’ theory of cancer metastasis. This theory has led to previous researchers focusing on the role of a tumour as a cancer seed and antiangiogenesis agents as cancer soil fumigant; for the latter to be effective, it is important for them to be able to distinguish cancer cells from stromal cells. However, antiangiogenesis agents have not produced dramatic survival benefits in vivo. This may be related to their inability to destroy the supporting stroma that promote cancer cell growth. Therefore, in order to effectively arrest cancer cell growth for therapeutic purposes, a paradigm shift is required in our fundamental approach to decipher the molecular events and networks in the stromal environment that cancer cells can thrive and proliferate. The pathogenesis of cancer is a multidimensional process of pathological molecular and cellular pathways, influencing different stromal properties and achieving a mutually negotiated crosstalk between cancer cells and stromal cells. This review summarises the clinical presentation of current knowledge of classical papillary thyroid carcinoma (PTC), emerging molecular diagnostics and future directions of classical PTC research.

Fibrin and Cancer Cell Growth: Problems in the Evaluation of Experimental Models

1979 ◽  
Author(s):  
Andreina Poggi
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Primary Tumour ◽  
Antiplatelet Agent ◽  
Experimental Models ◽  
Surgical Removal ◽  
Antiinflammatory Drugs ◽  
Cancer Cell Growth ◽  
Lung Carcinoma Cells

Studies on the role of fibrin in experimental cancer growth should take into account the following problems: 1) during growth and dissemination of experimental tumours, haemostatic changes may occur which vary depending on the route of inoculation of cancer cells and on the tissue wherethe tumour grows. Thrombocytopenia, haemolytic microangiopathic anaemia and decreased survival of fibrinogen were observed during spontaneous dissemination to the lung of i.m. implanted Lewis Lung Carcinoma cells, not when metastatic growth occurred after surgical removal of the primary tumour or lung nodules developed following i.v. injection of the same cells. 2) Treatment of experimental tumours with drugs active on the haemostatic system may have different effects depending on the stage of growth of the tumour. This observation (which we have made with both warfarin and a defibrinating enzyme in murine metastasizing tumours) could suggest that fibrin may play different roles at different phases of cancer cell growth. 3) The supposed antiturooral activity of drugs active on the haemostatic system may be also influenced by other factors, such as a direct activity on cancer cells or on the host’s immune system or on blood supply to the tumour. As an example, non steroidal antiinflammatory drugs may act not only as antiplatelet agent but also as inhibitors of prostaglandin synthesis by cancer cells and some snake venoms may influence cancer cell growth not only through defibrination, but also with their iinnu-nodepressant properties. (Supported by Italian CNR and NIM. MCI, USA).

192 RESVERATROL, A NATURAL FOOD COMPOUND, SUPPRESSED THE CELL GROWTH OF BG-1 OVARIAN CANCER CELLS INDUCED BY 17β-ESTRADIOL OR BISPHENOL A THROUGH DOWNREGULATING ESTROGEN RECEPTOR α AND INSULIN-LIKE GROWTH FACTOR-1 RECEPTOR

2013 ◽  
Vol 25 (1) ◽  
pp. 245
Author(s):  
N.-H. Kang ◽  
K.-C. Choi
Keyword(s):  
Ovarian Cancer ◽  
Growth Factor ◽  
Cell Growth ◽  
Bisphenol A ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Insulin Like Growth Factor ◽  
Cancer Cell Growth

Resveratrol (trans-3,4,5-trihydroxystilbene; RES) was adopted in this study as a novel phytoestrogen displaying antioxidant, antiinflammatory, and anticancer effects. In this study, we evaluated the inhibitory effect of RES on the cell growth induced by 17β-oestradiol (E2), a typical oestrogen, and bisphenol A (BPA), an endocrine-disrupting chemical (EDC) in BG-1 ovarian cancer cells expressing oestrogen receptors (ER) through down-regulating oestrogen receptor α (ERa) and insulin-like growth factor-1 receptor (IGF-1R). The EDC and oestrogen appear to promote the development of the oestrogen-dependent cancers. Thus, we need to develop therapeutic methods for EDC-dependent cancers. In in vitro experiments, we examined the cell viability and mRNA expression of ERa ± IGF-1R genes following the treatments with E2 or BPA in the presence or absence of RES or ICI 182 780, an ER antagonist, by MTT assay and RT-PCR, respectively. We also examined the protein level of ERa, phosphorylated insulin receptor substrate-1 (IRS-1), phosphorylated Akt1/2/3, p21, and cyclin D1 by Western blot analysis. Treatment with E2 or BPA remarkably increased the growth of BG-1 ovarian cancer cells, and their enhanced cell growth appeared to be mediated by ERa. In addition, the treatment of BG-1 ovarian cancer cells with E2 or BPA resulted in an increase in ERa and IGF-1R gene expressions. However, co-treatment of RES reversed E2- or BPA-induced ovarian cancer cell growth and mRNA expressions of ERa and IGF-1R. The protein levels of phosphorylated IRS-1 and Akt were upregulated by E2 or BPA, whereas these levels were downregulated by co-treatment of RES in the presence of E2 or BPA. Taken together, these results indicate that RES may effectively inhibit ovarian cancer cell growth via downregulating cross-talk between ERa and IGF-1R. This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Ministry of Education, Science and Technology (MEST) of Korea government (no. 2011-0015385).

scholarly journals Estrogen-induced epigenetic silencing of FTH1 and TFRC genes reduces liver cancer cell growth and survival

Epigenetics ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. 1302-1318
Author(s):  
Jibran Sualeh Muhammad ◽  
Khuloud Bajbouj ◽  
Jasmin Shafarin ◽  
Mawieh Hamad
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cell ◽  
Epigenetic Silencing ◽  
Liver Cancer Cell ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Cell Growth And Survival

scholarly journals Novel 2-step synthetic indole compound 1,1,3-tri(3-indolyl)cyclohexane inhibits cancer cell growth in lung cancer cells and xenograft models

Cancer ◽  
2008 ◽  
Vol 113 (4) ◽  
pp. 815-825 ◽  
Author(s):  
Ching-Hsiao Lee ◽  
Ching-Fa Yao ◽  
Sin-Ming Huang ◽  
Shengkai Ko ◽  
Yi-Hung Tan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Cancer Cell Growth ◽  
Indole Compound ◽  
Xenograft Models
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