Cell Cycle Regulators in Cancer: A Review | Chapter 11 | Achievements and Challenges of Medicine and Medical Science Vol. 4

A recent in-depth view of cell cycle regulation and cancer has provided novel samples of research at the “Frontiers of Science.” However, the number of foremost revealing information about both topics has been derived from the intersection of these two fields. Genomic integrity is required to maintain long life and prevent diseases associated with genomic instability such as “cancer.” The cell cycle is a compilation of well-organized, sequential molecular events, that lead to succession of DNA replication and segregation of replicated chromosomes. Checkpoint is an important control point present in the cell cycle where stop and start signals can regulate the cell cycle. Cell cycle checkpoints are the strict regulatory mechanisms that monitor the order, integrity, and fidelity of the main events of the cell cycle. These include growth up to the acceptable cell size, replication, and integrity of the chromosomes, and their accurate segregation in due course of mitosis. Many of these mechanisms are highly conserved, while other studies on higher organisms have shown to control alternative cell fates with a significant impact on tumor suppression. Here, these different checkpoint pathways in a cell cycle and the consequences of their dysfunction on the fate of a cell has been taken into consideration. Undoubtedly, the hidden aspects of checkpoint signaling can be further explored with the help of an ever-growing arsenal of highly sophisticated experimental tools and techniques, which will enable us to get a more clear and complete picture of the remarkable fidelity of the cell cycle.

 

Author (s) Details

Swarup K Panda
Department of Biochemistry, IMS & SUM Hospital III, Sitalapalli, Ganjam, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Subhashree Ray
Department of Biochemistry, IMS & SUM Hospital, K8, Kalinga Nagar, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Sarthak R Nayak
Department of Biochemistry, IMS and SUM Hospital II, Phulnakhara, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Sudeshna Behera
Department of Biochemistry, IMS & SUM Hospital, K8, Kalinga Nagar, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Sangeeta S Bhanja
Department of Biochemistry, IMS & SUM Hospital, K8, Kalinga Nagar, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Viyatprajna Acharya
Department of Biochemistry, KIMS, KIIT (Deemed to be University), Bhubaneswar, Odisha, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/acmms/v4/3165 

Methyl Donors Inhibit Panc-1 Cell Proliferation by Decreasing NFkB and Erk Signaling Levels and Raising E-Cadherin Expression | Chapter 11 | Current Practice in Medical Science Vol. 8

The physiology of cancer patients, particularly those with pancreatic cancer, may be improved by dietary methyl donors, which may also be utilised as intervention treatment. In this study, an aggressive pancreatic adenocarcinoma cell line (Panc-1) was treated with methyl-donors (L-methionine, choline chloride, folic acid, and vitamin B12), which significantly increased the levels of p21WAF1/Cip1 cyclin dependent kinase inhibitor and the SubG1 fractions while significantly decreasing the levels of phospho-Erk1/2 and the proliferation rate. Diet is one of the lifestyle-related factors in the genesis of pancreatic cancer, an aggressive malignancy with a high chance of metastasizing. Methyl-donors are dietary micronutrients that function as bioactive food ingredients by delivering methyl groups as cofactors and substrates for critical metabolic pathways. Pathological disorders have recently been related to methyl-donors' unbalanced nutritional status. Although Bak, Puma, and Caspase-9 levels were likewise raised by methyl donor treatments, cleaved Caspase-3 levels were not. The production of the transcription factor NFkB and the pro-inflammatory cytokine IL-17a was also markedly decreased by the therapy. After methyl-donor treatments, SDF-1a and VEGF levels were found to be much lower, which may indicate a reduced risk of metastatic dissemination. As was anticipated, E-cadherin expression increased following the methyl-donor therapy and was negatively correlated with these changes. It is determined that methyl-donors may have the ability to lessen Panc-1 cells' aggressive and proliferative character. This implies a potential function for dietary methyl-donors in enhancing

 

Author (s) Details

Eva Kiss

Department of Internal Medicine and Oncology, Oncology Profile, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

 

Gertrud Forika

Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, 1085 Ulloi u 26, Hungary.0

Istvan Takacs

Department of Internal Medicine and Oncology, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

Tibor Krenacs

Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, 1085 Ulloi u 26, Hungary.

Zsuzsanna Nemeth

Department of Internal Medicine and Oncology, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

 

Please see the link here:-  https://stm.bookpi.org/CPMS-V8/article/view/7800

Inhibition of 6-Methylsulfinylhexyl Isothiocyanate for Cell Cycle Progression in Quiescent JB6 Cells Stimulated with Fetal Bovine Serum, Accompanied by Suppression of Cyclin A2 Expression | Chapter 5 | New Innovations in Chemistry and Biochemistry Vol. 5

 Wasabi contains a chemical called 6-Methylsulfinyhexyl isothiocyanate (6-MSITC) (Wasabia japonica Matsumura). In quiescent JB6 cells, 6-MSITC inhibited cell cycle progression when activated with epidermal growth factor. The goal of this work is to look into the mechanism of 6-MSITC's inhibitory effects on cell cycle progression induced by foetal bovine serum (FBS). In serum-starved JB6 cells for 36 hours, 6-MSITC reduced FBS-stimulated cell cycle advancement. Treatment with 6-MSITC, on the other hand, had no effect on Rb protein, cyclin D1, cyclin D2, cyclin D3, CDK4, CDK6, p16, p21, and p27, as well as cell growth signalling via the Akt and MAPK pathways. 6-MSITC, on the other hand, reduced DNA polymerase activity by inhibiting gene expression in DNA synthesis-related proteins such cyclin A2. These findings show that 6-MSITC suppresses FBS-stimulated cell cycle progression from G0 to S phase in quiescent JB6 cells, as well as suppressing cyclin A2 gene expression.

Author(S) Details

Takashi Hashimoto
Division of Applied Chemistry in Bioscience, Graduate School of Agricultural Science, Kobe University, Rokkodai-cho 1-1, Nada-ku, Kobe 657-8501, Japan.

Maki Kobayashi
Division of Applied Chemistry in Bioscience, Graduate School of Agricultural Science, Kobe University, Rokkodai-cho 1-1, Nada-ku, Kobe 657-8501, Japan and Faculty of Nutrition, Kobe Gakuin University, 518 Arise, Ikawadani, Nishi, Kobe, Hyogo 651-2180, Japan.

Kazuki Kanazawa
Division of Applied Chemistry in Bioscience, Graduate School of Agricultural Science, Kobe University, Rokkodai-cho 1-1, Nada-ku, Kobe 657-8501, Japan.

View Book:- https://stm.bookpi.org/NICB-V5/article/view/5146