Publications by authors named "Pablo Perez-Ramos"
Article Synopsis
- The colonic epithelium’s exposure to bile acids, particularly deoxycholic acid (DCA) and chenodeoxycholic acid (CDCA), can lead to cytotoxic effects linked to colon cancer development.
- Both DCA and CDCA induce cell death in colon cancer cells, with CDCA being more effective, and trigger apoptosis through various mechanisms such as mitochondrial dysfunction and oxidative stress.
- The apoptosis process involves increased reactive oxygen species (ROS), loss of mitochondrial potential, activation of caspases (notably caspase-9 and -3), and changes in apoptotic proteins like Bcl-2 and Bax, ultimately amplifying cell death signals.
A controlled balance among cell proliferation, differentiation, and apoptosis is required for the maintenance of gastrointestinal mucosa; these processes are influenced by luminal components, such as butyrate and bile acids. Using butyrate-sensitive (BCS-TC2) and butyrate-resistant (BCS-TC2.BR2) human colon carcinoma cells, we wanted to establish whether colon carcinoma cells that acquire resistance to butyrate-induced apoptosis are also resistant to the cytotoxic effect of certain bile acids, contributing, in this way, to the progression of colon carcinogenesis.
View Article and Find Full Text PDFButyrate induces differentiation and alters cell proliferation in intestinal-epithelial cells by modulation of the expression of several genes. Annexins are a superfamily of ubiquitous proteins characterized by their calcium-dependent ability to bind to biological membranes; their involvement in several physiological processes, such as membrane trafficking, calcium signaling, cell motility, proliferation, and differentiation has been proposed. Thus, we have analyzed changes in annexin A1 (AnxA1), annexin A2 (AnxA2), and annexin A5 (AnxA5) levels and localization in human colon adenocarcinoma cells differentiated by butyrate treatment or by culture in glucose-free inosine-containing medium.
View Article and Find Full Text PDFAcquired resistance to apoptosis by tumor cells remains a major obstacle for cancer treatment, and hence the analysis of resistance to apoptosis constitutes a major goal in the development of antitumoral drugs. We have established a butyrate-resistant human colon adenocarcinoma cell line (BCS-TC2.BR2) from nontumorigenic BCS-TC2 cells to analyze whether the acquisition of such phenotype confers resistance to apoptosis and stress.
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