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Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Oncogenes are homologs of normal genes that typically have a role in cell cycle regulation and cell growth pathways. A mutation in an oncogene may result in consecutive activation of that gene, leading to uncontrolled cellular proliferation [13]. Among the oncogenes, the RAS oncogene is implicated in cancer development. This oncogene exists in three variants on the cellular level, HRAS, KRAS, and NRAS. When mutated, all these three oncogenes are able to transform normal cells into cancer cells. However, in colorectal cancer, KRAS is the most frequently mutated [14, 15].
Carrier Screening For Inherited Genetic Conditions
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Whitney Bender, Lorraine Dugoff
Clinical features: This disease is caused by disruption to normal DNA repair mechanisms, resulting in genomic instability, abnormal cell cycle regulation, and cell death. Clinical features include congenital anomalies such as thumb or other radial ray anomalies, microcephaly, and facial or renal abnormalities. Affected children are predisposed to short stature, bone marrow failure, and leukemia and other cancers.
The Fight Against Cancer
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
Abnormalities in cell cycle regulation may occur at any of the four major phases, known as G1, S, G2, and M. progression through these phases of the cell cycle depends on the balance of the chemical signals that promote growth or inhibition. The G1 (gap 1) phase is where the cell grows in size and prepares for DNA replication in response to growth factors. The second phase (synthesis) is when DNA replication takes place. The next interval, once the chromosomes have been copied, is G2 phase (gap 2) where the cell prepares for division. During this interval, the cell has time to check for errors in the DNA replication, and repair any damaged copies. The final phase, M (mitosis) is when cell division happens to produce two daughter cells, each containing a full set of chromosomes. The daughter cell then begins the cell cycle at the G1 phase, or may remain in a dormant phase G0.
The role of CSE1L silencing in the regulation of proliferation and apoptosis via the AMPK/mTOR signaling pathway in chronic myeloid leukemia
Published in Hematology, 2023
Xiao-Yu Liu, Yong-Hong Wang, Jing Wang, Ji-Kun Quan, Xu-Dong Li, Kun-Ping Guan
CSE1L has been reported to play an important role in maintaining the balance between cell proliferation and apoptosis [6,28]. Cancer development and survival need CSE1L [29]. Inhibition of CSE1L expression has been shown to slow the growth and spread of triple-negative breast cancer [30]. Silencing CSE1L inhibits the viability of lung cancer cells and reduces malignant transformation of cancer cells [31]. However, no studies on the expression of CSE1L in CML have been done. To investigate the possible molecular mechanism of CSE1L expression in CML patients, we detected the relative expression level of CSE1L in bone marrow granulocytes by flow cytometry. The results showed that strong CSE1L signals were detected in bone marrow granulocytes from patients with primary CML. In a K562 cell model,we showed that knockdown of CSE1L shifts K562 cells from low Annexin to medium Annexin levels. This result confirmed that knockdown of CSE1L can reduce the growth of K562 cells and induce apoptosis. Disruption of cell cycle checkpoints has been identified as a hallmark of cancer, with the G1-S phase being the most important regulatory point in cell cycle regulation [32,33]. In our study, knockdown of CSE1L also hindered the cell cycle transition from G0/G1 phase to the S phase, without significant effect on the G2/M phase. Interestingly, our study showed that imatinib triggered a downregulation of CSE1L in K562 cells. The results suggest that CSE1L is involved in imatinib-induced killing of K562 cells. The findings suggest that CSE1L may play a significant role in the onset and progression of CML.
Polysaccharides from Hemerocallis citrina Baroni Inhibit the Growth of Hepatocellular Carcinoma Cells by Regulating the Wnt/β-Catenin Pathway
Published in Nutrition and Cancer, 2023
TianYu Sang, Yue Jun Fu, Li Song
The cell cycle is a precisely regulated process that ensures genetic integrity during cell division. Tumor cells are characterized by abnormal cell cycle regulation. Therefore, some antitumor drugs inhibit tumor cell proliferation by modulating the cell cycle and causing cell cycle arrest (29, 30). Our results showed that polysaccharides HcBPS2 significantly inhibited HCC cell proliferation and induced cell cycle arrest in G2/M phase. G2/M phase is an important DNA damage checkpoint. When a cell with DNA damage cannot repair the damage present, the G2/M phase checkpoint prevents the cells from entering M phase (31). Cyclin B1 regulates the transformation from G2 to M phase. Cyclin B1 can bind with the cell cycle-dependent kinase Cdc2 and then promote the cell cycle (16). Cyclin D1 is a crucial regulator during G2 phase (32). Cyclin D1 levels are elevated during G2 phase, which allows the cell to enter the next cycle (32). P21 is a cyclin-dependent kinase inhibitor that promotes G2/M phase arrest by inhibiting the expression of Cdc2 (33). This study found that the level of P21 was significantly increased and the expression levels of cyclin B1 and cyclin D1 were notably decreased in HcBPS2-treated cells. These findings suggested that cyclin B1, cyclin D1 and P21 were involved in HcBPS2-induced G2/M phase arrest.
GC-MS Profiling and Antineoplastic Activity of Pelargonium Inquinans Ait Leaves on Acute Leukaemia Cell Lines U937 and Jurkat
Published in Nutrition and Cancer, 2022
Ogochukwu Izuegbuna, Gloria A. Otunola, Graeme Bradley
Cell cycle regulation was also investigated in this study. The extracts of Pelargonium inquinans were observed to cause G1 cell cycle arrest in both Jurkat and U937 cell lines. This is related to similar findings in P. sidoides by Perreira et al20. The G1 phase is usually characterized by protein synthesis toward cell division. In a recent study, cancer cells were observed to migrate more rapidly in the G0/G1 phase than in the S/G2/M phase; they were also more resistant to cytotoxic drugs in the G0/G1 phase21. Thus targeting the G1 phase of the cell cycle is seen as a viable option in cancer management22. Flavopiridol, a flavonoid, and a pan-CDK inhibitor showed significant activity in chronic lymphoid leukemia, though with overt toxicities23. Cell cycle progression in the G1 phase is regulated by CDK 4 and six and palbociclib a CDK4/6 inhibitor have been shown to have activity in acute myeloid leukaemia24. A Phase I/II clinical trial of palbociclib and CPX-351 is currently ongoing (NCT03844997). Dinaciclib a CDK9 inhibitor that also promotes apoptosis in MLL-rearranged AML is also currently being evaluated with some other drugs in AML in some clinical trials (NCT03484520); (NCT02684617). Thus, cell cycle inhibitors can be viable options in the management of AML.