Genetics of prostate cancer
J. K. Cowell in Molecular Genetics of Cancer, 2003
MYC. Gain of 8q in prostate cancers was first described by Bova et al., (1993). Gain of 8q is more prevalent in recurrent tumors (Visakorpi et al., 1995a) as well as in metastatic lesions (Cher et al., 1996) than in primary tumors. Accordingly, 8q gains are associated with a short progression-free interval (Takahashi et al., 1994), and the presence of lymph-node metastasis (Van Den Berg et al., 1995). The MYC oncogene is located at 8q24, the other of the minimally amplified regions at 8q (Cher et al., 1996; Nupponen et al., 1998; Visakorpi et al., 1995a). This well-known oncogene plays an important role in the regulation of cellular proliferation, differentation, and apoptosis (reviewed in Henrikksson and Lucher, 1996). Both over-expression and amplification of MYC have been detected in prostate tumors (Buttyan et al., 1987; Fleming et al., 1986; Nupponen et al., 1998). However, relatively few prostate tumors show high-level amplification of MYC (Bubendorf et al., 1999; Nupponen et al., 1998), indicating that there may exist other target genes for the 8q23–24 amplification, in addition to those at the other minimally amplified region 8q21. MYC is, however, suggested to play an important role in metastatic prostate cancer (Bubendorf et al., 1999).
Cellular Oncogenes as Biotherapeutic Targets for the Differentiation and Inhibition of Cancer Cells
Robert I. Glazer in Developments in Cancer Chemotherapy, 2019
Recent studies have determined that several cellular oncogene products are closely related to growth factor receptors (Figure 3). The v-sis oncogene product resembles platelet-derived growth factor (PDGF), which plays an important role in wound healing.85,86 Similarly, the human EGF receptor is closely related to the product of the v-erb B oncogene. In the latter instance, the overproducing epidermoid carcinoma cell line A431 has been used almost exclusively to study the EGF receptor tyrosine protein kinase87-93 and the messenger RNAs94-96 encoding the normal and aberrant EGF receptor in these cells. This cell line is also the only one thus far possessing amplified receptor-gene sequences and an aberrant truncated form of the EGF receptor which is devoid of tyrosine protein kinase.97 Although the latter mutant EGF receptor can be considered a result of a rearrangement and amplification in the gene, its presence has not provided any clue to the neoplastic properties of this cell line.
Driver Mutations
John Melford in Pocket Guide to Cancer, 2017
In 1969, Robert J. Huebner and George J. Todaro, working at the U.S. National Cancer Institute, coined the term oncogene to refer to viral information including “that portion responsible for transforming a normal cell into a tumor cell.” Despite regular use of the term and recent advances in our understanding of the genetic causes of cancer, there are many different definitions of an oncogene, some of which are not quite accurate. For example, an oncogene is often defined as a mutated gene that turns cell division on, which excludes genes that are over expressed such as the HER2 gene in breast cancer. Some definitions unwittingly include TSGs, while others do not make it clear that an oncogene may be a mutated form of a normal gene.
Targeted therapy of tumour microenvironment by gold nanoparticles as a new therapeutic approach
Published in Journal of Drug Targeting, 2022
Negah Mahhengam, Kimia Kazemnezhad, Hendrik Setia Budi, Mohammad Javed Ansari, Dmitry Olegovich Bokov, Wanich Suksatan, Lakshmi Thangavelu, Homayoon Siahmansouri
Beta-catenin (β-catenin) is a dual function protein with a coordination task in physiological homeostasis. Its unusual expression results in severe diseases, including cancer. Naturally, beta-catenin helps maintain the integrated structure of epithelial tissue and controls the transcription of various genes through extracellular agents. β-catenin operates as a part of the cadherin protein complex in the epithelial tissues and adjusts intracellular adhesion and epithelial cell development. In Wnt signalling, beta-catenin is the primary transcriptional regulator and plays a pivotal role in stem cell renewal, embryogenesis, and organ repair. What is more, the Improper expression of beta-catenin leads normal cells to become malignant. As mentioned earlier, this protein can act as a transcription modifier and oncogene to induce cancer, development of malignant cells, survival, and relapse. For these reasons, researchers have considered beta-catenin as one of the ideal targets for drug delivery [151].
Upregulation of lncRNA H19 promotes nasopharyngeal carcinoma proliferation and metastasis in let-7 dependent manner
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Yujie Zhang, Ronghua Zhu, Jia Wang, Zheqing Cui, Ying Wang, Yulin Zhao
LncRNA H19 features in the exclusive expression from the maternal allele. The product of this gene is increasingly recognized as oncogene in range of human cancers. For example, the study performed by Luan et al. reported that H19 promoted glucose metabolism and cell growth in malignant melanoma via miR-106a-5p/E2F3 axis [11]. Liang et al. demonstrated that sTLR4/MD-2 complex inhibited colorectal cancer migration and invasiveness in vitro and in vivo by lncRNA H19 down-regulation [12]. Yan et al. suggested that H19/miR-675 axis promoted gastric cancer via FADD/Caspase 8/Caspase 3 signalling pathway [13]. In respect to nasopharyngeal carcinoma, Ng et al. disclosed the regulation of H19 imprinting gene expression by promoter hypomethylation [14]. More importantly, Li et al. demonstrated that H19 regulated EZH2 expression by interacting with miR-630 and promoted cell invasion [15]. However, the credibility of this study is evidently compromised by the sole experiment with cell culture in vitro. Therefore, here we sought to revisit this subject via employment of nasopharyngeal carcinoma xenograft mice model and prepared to unravel the underlying mechanisms.
circYap inhibits oral squamous cell carcinoma by arresting cell cycle
Published in Acta Odontologica Scandinavica, 2022
Xiao-Yun Zhang, Huifang Tang, Yanping Liu, Nan Du, Songbo Tian, Yong-Qing Dou
Then circYap were overexpressed in CAL-27 cells and knocked down in SSC-4 cells. BrdU assay confirmed that overexpression of circYap could significantly inhibit the proliferation of CAL-27 cells, while knockdown of circYap could significantly promote the proliferation of SSC-4. The results proved that circYap inhibited the proliferation of OSSC cells. Proliferating Cell Nuclear Antigen (PCNA) can regulate cell proliferation and is a prognostic marker for malignant tumors [21]. C-MYC protein, the translation product of oncogene c-MYC gene, promotes cell division and regulates cell proliferation [22]. We detected the expression of two proteins. The results showed that overexpression of circYap significantly inhibited the expression of PCNA and C-MYC proteins, while knockdown of circYap significantly promoted the expression of PCNA and c-MYC proteins. The results further confirmed the inhibitory effect of circYap on the proliferation of OSSC cells.
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