China
Africa
Explore chapters and articles related to this topic
Chemical Causes of Cancer
Published in Peter G. Shields, Cancer Risk Assessment, 2005
Gary M. Williams, Alan M. Jeffrey
Each type of malignancy has a specific pattern of metastasis which is determined both by lymphatic and blood drainage from the tumor, and also by factors produced by disseminated cells allowing them to establish metastases (157,158). Genes regulating metastasis of tumor cells have been categorized as either metastasis-promoting (CDH2, CXCRy, MTA1) or metastasis-suppressing (CD9, CD44, Nm 23, KiSS1, Ka11/CD82, CDH1,MAP2K4, MKK4, TIMP, and BRMS1) (159). Several of these (CD9,CD44, and CD82) code for transmembrane proteins. One possible mechanism for metastasis inhibition is the maintenance of gap junction intracellu-lar communication (160).
Fruit and Vegetable Consumption and the Risk of Prostate Cancer: A Systematic Review and Meta-Analysis
Published in Nutrition and Cancer, 2022
Huaqing Yan, Xiaobo Cui, Peng Zhang, Rubing Li
The potential molecular mechanisms of fruit and vegetable consumption and the prevention of PCa has remained poorly understood. Because the association between diet and PCa is complex, most basic researches focused on only fruit and vegetable extracts. It is reported that grape seed extract inhibited the cell viability and migration in DU145 and PC3M cells through downregulating metastasis-associated protein 1 (MTA1), a critical component of the nucleosome remodeling and histone deacetylase complex (25). MTA1 is localized to the nucleolus and regulates pre-rRNA transcription to promote cancer cell malignancies (26). Sinapic acid, an extract from various vegetables and fruit species, is reported to inhibit PCa cell viability and metastasis by increasing caspase-3 activity and downregulating MMP-9. The discrepancy between experimental studies and cohort studies may due to the following reasons: a) The totally different study design; b) The study subjects are people and PCa cells respectively; c) The exposure and outcome assessment are different; d) Cohort studies require years long follow-up time while experimental studies not. The relationship of fruit and vegetable consumption and the risk of PCa still remains unclear and more basic experimental studies should be performed to further elucidate the possible molecular mechanism of fruit and vegetable consumption and the risk of PCa.
Impact of laparoscopy on the biological behavior and gene expression of endometrial adenocarcinoma cells
Published in Gynecological Endocrinology, 2017
Shouguo Huang, Jie Qin, Jin Chen, Hong Cheng, Qiu Meng, Jing Zhang, Haiyan Wang
MTA1 was first isolated from a metastatic breast cancer cell line and has since been shown to be upregulated in several other metastatic human cancers. MTA1 has been demonstrated [21–23] to regulate cell growth and tumor metastasis through modifying histone proteins, encoding transcriptor, participating in the signal transduction pathways and mediating the expression of related genes. Elevated expression levels of MTA1 are strongly associated with tumors characteristic of high serosa infiltration, elevated lymph node dissemination and strong vascular invasion [22–25]. In the present study, MTA1 was expressed in a significantly higher level in the endometrial adenocarcinoma cells before laparoscopy. And the expression of nm23-H1 in the endometrial adenocarcinoma cells was elevated after laparoscopy with a statistical significance. Meanwhile, there were no significant difference in the expressions of MTA1 and nm23-H1 of the endometrial adenocarcinoma cells in the laparotomy group. Interestingly, MTA1 and nm23-H1 were not regulated by laparoscopy in the normal endometrial cells. In the endometrial adenocarcinoma cells, the expression of MTA1 was higher after laparoscopy than that after laparotomy; nm23-H1 was lower expressed in the post-laparotomy group when compared with that in the post-laparoscopy group. Herein, it is suggested that down-regulation of MTA1 and up-regulation of nm23-H1 are induced by laparoscopy in the endometrial adenocarcinoma cells instead of normal endometrial cells. Still, laparotomy will bring no effect on the expression of MTA1 and nm23-H1 in the endometrial adenocarcinoma cells.
MTA1 promotes the invasion and migration of pancreatic cancer cells potentially through the HIF-α/VEGF pathway
Published in Journal of Receptors and Signal Transduction, 2018
Xianchun Sun, Yan Zhang, Bingshu Li, Haiyan Yang
The metastasis-associated gene 1 (MTA1), which is an necessary ingredient of the nucleosome remodeling and histone deacetylation (NuRD) complex [5,6], has been considered to be a critical regulator of the carcinogenesis and metastasis of a variety of human cancers including non-small cell lung cancer [7,8], nasopharyngeal carcinoma [9,10], prostate cancer [11,12], breast cancer [13,14]. The MTA1 proteins modulate the procedure of tumor progression and metastasis, including transformation, anchorage-independent cell growth, invasion, epithelial-mesenchymal transition, survival, DNA repair, angiogenesis, inflammation, metastasis, and chemo-resistance [5,15]. However, the role of MTA1 in the metastasis of pancreatic cancer remains unclear.