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Molecular genetics of lung cancer
Published in J. K. Cowell, Molecular Genetics of Cancer, 2003
Frederic J. Kaye, Akihito Kubo
The recognition that the viral transforming proteins from adenovirus, simian virus 40 (SV40), and human papillomavirus (HPV) could precipitate the RB1 product led to a model where RB tumor suppressor function is mediated through a ‘pocket’ protein-binding activity (Weinberg, 1995). In addition to RB1, however, several other protein species are co-precipitated by the same viral transforming proteins (Whyte et al., 1989). Two of these unknown species were initially designated as pl07 and pl30 according to their apparent molecular weights on SDS-PAGE gels. The subsequent isolation of these genes revealed that they were highly related to RB1, especially in the central domains that are responsible for generating the ‘pocket’ protein binding function (Ewen et al., 1991; Li et al., 1993; Mayol et al., 1993). The roles of the RB-related 1 gene (RBL1/pl07) and the RB-related 2 gene (RBL2/pl30), however, are still undefined (Kaye, 1998). Ectopic expression of all three RB1-related gene members results in growth suppression of mammalian cells and it has been suggested that inactivation of RBL1 and RBL2 may be required in vitro to manifest the fully transformed phenotype even in RB1−/− cells. In contrast to the RB1 gene, however, mutational inactivation of these RB1-related genes has not, until recently, been observed in human tumor samples. In 1997, investigators reported that 1/19 SCLC cell lines showed inactivation of the RBL2/p130 gene (Helin et al., 1997). Subsequently other investigators reported that approximately 30% of non-SCLC had altered expression of RBL2 by immunohistochemistry which was associated with a worse clinical outcome (Baldi et al., 1997). In addition, these authors have reported an unusual clustering of mutations in a wide range of human tumors predominantly within the carboxy-terminal exons of RBL2 (Cinti et al., 2000; Claudio et al., 2000a). For example, they reported that 11/14 lung cancer samples showed multiple missense and frameshift RBL2 mutations (Claudio et al., 2000b). In contrast, however, we have not identified mutational inactivation in either the RBL1/p107 or the RBL2/p130 gene in a large collection of SCLC and non-SCLC tumor cell lines (Modi et al., 2000). Therefore, while simultaneous inactivation of multiple RB-related family members in lung cancer is an important hypothesis, the role of RBL1 and RBL2 is still undefined.
A Marine Carotenoid of Fucoxanthinol Accelerates the Growth of Human Pancreatic Cancer PANC-1 Cells
Published in Nutrition and Cancer, 2022
Masaru Terasaki, Shouta Takahashi, Ryuta Nishimura, Atsuhito Kubota, Hiroyuki Kojima, Tohru Ohta, Junichi Hamada, Yasuhiro Kuramitsu, Hayato Maeda, Kazuo Miyashita, Mami Takahashi, Michihiro Mutoh
The 44 up-regulated genes in FxOH-treated PANC-1 cells co-existed in more than five gene pathways based on the TAC analysis, namely, a pathway-based gene profile (Table 3). Fourteen genes, namely, DDIT3, CCND2, FYN, GRB10, VEGFA, CEBPB, ATF4, GATA3, PRKACB, SQSTM1, NFATC1, IFRD1, FGF2, and HBEGF, belonged to the gene sets involved in the promotion of cell growth, cell cycle, adhesion, and inflammation. Particularly, FYN and VEGFA were involved in 32 and 36 gene sets, respectively, in PANC-1 cells. The 52 down-regulated genes in FxOH-treated PANC-1 cells co-existed in more than five gene sets based on the TAC analysis (Supplementary Table S1). Four genes, WEE1, CHEK1, RBL1, and BIRC5, belonged to the gene pathways involved in the suppression of the cell cycle and apoptosis. The 43 up-regulated genes in FxOH-treated DLD-1 cells co-existed in more than five gene pathways based on the TAC analysis (Supplementary Table S2). Eighteen genes belonged to the gene sets involved in the suppression of the cell cycle, cell growth and inflammation, and the enhancement of apoptosis. The 38 down-regulated genes in FxOH-treated DLD-1 cells co-existed in more than five gene sets based on the TAC analysis (Supplementary Table S3). Twenty-four genes belonged to the gene sets involved in the promotion of the cell cycle, cytoskeleton remodeling, DNA repair, cell growth, and inflammation.
Evolutionary Underpinnings of Innate-Like T Cell Interactions with Cancer
Published in Immunological Investigations, 2019
Maureen Banach, Jacques Robert
Since all multicellular organisms are susceptible to tumors, it is not surprising that a range of spontaneous tumors have been described in Xenopus (Robert, 2010; Stern et al., 2014). However, deriving tumor cell lines from these cancers has been met with little success. The induction of cancers with potent carcinogens, such as N-dimethylnitrosamine or N-methyl-N-nitrosourea, that in mice cause extensive DNA damage, have resulted in limited carcinogenesis in Xenopus (Balls et al., 1989, 1983). Reverse genetic methodologies to disable gene function have recently propelled the development of tumors in Xenopus. For instance, Transcription Activator-Like Effector Nucleases (TALEN)-mediated disruption of the tumor suppressor gene adenomatous polyposis coli apc gene in X. tropicalis was reported to lead to familial adenomatous polyposis, similar to mouse and human intestinal cancers (Van Nieuwenhuysen et al., 2015). Also, akin to pediatric tumors of retina, double knockouts of retinoblastoma 1 (rb1) and retinoblastoma-like 1 (rbl1) by the clustered regularly interspaced short palindromic and associated protein 9 nuclease (CRISPR/Cas9) technology initiated retinoblastoma in X. tropicalis (Naert et al., 2016).
Identification of Potential Therapeutic Genes and Pathways in Phytoestrogen Emodin Treated Breast Cancer Cell Lines via Network Biology Approaches
Published in Nutrition and Cancer, 2022
Elif Sakalli-Tecim, Pembegul Uyar-Arpaci, N. Tulin Guray
In MDA-MB-231, the number of genes belonging to differentially regulated 5 pathways (Table 4) was found as 36. Among these, only eight genes were regulated in more than one pathway and as the most, five genes (CDK1, CCNB1, CCNB2, CCNE2, CHEK1) were regulated through three pathways namely cell cycle, p53 signaling pathway and cellular senescence. Three genes were regulated in two pathways (CCNA2 and RBL1 were regulated in both cell cycle and cellular senescence; MCM5 was regulated in cell cycle and DNA replication).