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Anti-Cancer Agents from Natural Sources
Published in Rohit Dutt, Anil K. Sharma, Raj K. Keservani, Vandana Garg, Promising Drug Molecules of Natural Origin, 2020
Debasish Bandyopadhyay, Felipe Gonzalez
Colicins are class III bacteriocins, originated from specific strains of the bacterium Escherichia coli or other similar Enterobacteriaceae (Feldgarden et al., 1999). The mechanism of action in bacterial cells has been studied, revealing that colicins have the potential to cause cell death through membrane translocation and cell binding. If colicins could kill bacterial cells, do they have the potential to destroy cancerous cells? A study conducted by Chumchalová (2003)to validate the effectiveness of four types of colicins viz. A, E1, E3, and U, on eleven types of malignant (human) cells and also in fibroblast cells that carried P53 gene mutations. The cell lines of interest were MRC5 (standard fibroblast, wild-type p53), MCF7, and ZR75 (breast carcinoma, wild-type p53). The following cell types had a detection of p53: breast carcinoma: BT549, BT474, MDA-MD-231, SKBR3, and T47D, colon carcinoma: HT29, osteosarcoma: HOS, leiomyosarcoma: SKUT-1, and fibrosarcoma: HS913T. The most promising colicins were colicin A and E1, as both showed inhibition of cellular growth to most of the tested cell lines. Colicine A showed 16–56% inhibition, while colicin E1 showed an inhibition of 17–40%. One problem with colicine A was that it also inhibited 36% of the normal MRC5 fibroblast cells. Colicine E3 and U showed no significant changes in cell cycles. Cell cycle was altered notably in cell lines HS913T and MRC5 produced by Colicin A.
Prospective Therapeutic Applications of Bacteriocins as Anticancer Agents
Published in Ananda M. Chakrabarty, Arsénio M. Fialho, Microbial Infections and Cancer Therapy, 2019
Lígia F. Coelho, Nuno Bernardes, Arsénio M. Fialho
Colicins are AMPs found in Enterobacteriaceae. Functionally, these molecules will confer to the producer organism some type of competitive advantage against other Enterobacteriaceae strains. Beside the antimicrobial activities colicins are known to have anticancer activities against a selection of human tumor cell lines in vitro, such as leukemia, breast cancer, colon cancer, bone cancer, and cervix cancer [15, 45]. Colicins A and E1 have been demonstrated to be cytotoxic against 11 different tumor cell lines with defined mutations of suppressor gene p53, with variations between 17% and 60% depending on the cell line and on the colicin used. Colicin A appeared also to be cytotoxic against the fibroblast normal cell line in contrast with colicin E1, which proved to be less cytotoxic against this normal cell line, giving preliminary confirmation of some type of selectivity. Colicin E1 showed 50% inhibition in fibrosarcoma and breast carcinoma cell lines, with inhibition ranges varying from 15% to 25% depending on the colicin used [43].
Bacteria and Bioactive Peptides
Published in Prakash Srinivasan Timiri Shanmugam, Understanding Cancer Therapies, 2018
Ameer Khusro, Chirom Aarti, Paul Agastian
Colicins are plasmid-encoded high molecular weight (>20 kDa) peptides secreted by Enterobacteriaceae. Colicins show anticancer activities against several human tumor cell lines such as breast cancer, colon cancer, bone cancer, and uteri cell line HeLa. Chumchalova and Smarda (2003) demonstrated the effects of four pure colicins—A, E1, U, and E3—on 11 human cancer cell lines using MTT (tetrazoliumbromide) assay, showing colicin E1 and A to be the most potent. In another report, colicin E3 exhibited complete killing of human uteri carcinoma cell line (Smarda et al. 1978). Colicin E3 also showed time- and dose-dependent anticancer activity against murine leukemia cells P388 (Fuska et al. 1978). The direct administration of colicin E3 into the subcutaneous nodes of solid HK-adenocarcinoma showed significant reduction in mean mass of tumor in mice (Cursino et al. 2002). The mode of action of colicins is not yet known, but a few studies reported that colicin E3 cleaves the 18S rRNA of the isolated eukaryotic ribosomes (Turnowsky et al. 1973; Suzuki 1978). Colicins kill cancer cells by creating pores in the plasma membrane, thereby activating apoptosis (Chumchalova and Smarda 2003).
Microbial adaptation to the healthy and inflamed gut environments
Published in Gut Microbes, 2020
Yijie Guo, Sho Kitamoto, Nobuhiko Kamada
Bacterial cooperation or competition with other bacteria are key elements for defining the bacterial fitness in the inflamed gut Figure 2c. DSS-induced intestinal inflammation is often accompanied by an alteration of the gut microbiota (i.e., dysbiosis). Metagenomic sequencing has revealed that bacterial formate oxidation and oxygen respiration are overrepresented metabolic pathways in the dysbiotic microbiome. E. coli uses microbiota-derived formate through oxygen respiration to enhance its fitness in the inflamed gut Figure 2c. 55 Colicins are bacterial protein toxins that show potent activity against sensitive strains in vitro. S. enterica ser. Typhimurium produces colicin Ib (ColIb), a narrow-spectrum protein toxin active against related Enterobacteriaceae, such as colicin-sensitive commensal E. coli.56 The inflammatory environment in the gut provides unique conditions that potentiate the effects of colicins. Neutrophils migrate into the lumen of the inflamed gut and release iron-depleting agents and reactive oxygen and nitrogen species. This significantly induces the genes for ColIb production in S. enterica ser. Typhimurium and its corresponding ColIb-surface receptor CirA in commensal E. coli. Hence, S. enterica ser. Typhimurium produces ColIb, which confers a growth advantage over commensal E. coli in the inflamed gut. In contrast, in the absence of gut inflammation, ColIb production does not confer a competitive advantage to S. enterica ser. Typhimurium.56 Abnormal mucus regulation is a hallmark of intestinal inflammation, linked to the expansion of pathogens. During DSS-induced colitis, the increased release of sialic acids from mucin is caused by the expansion of B. vulgatus, which produces a sialidase. Sialic acids are, in turn, incorporated into the bacterial capsule of Enterobacteriaceae, such as E. coli, thus enhancing fitness Figure 2c57,58
Non-antibiotic antibacterial peptides and proteins of Escherichia coli: efficacy and potency of bacteriocins
Published in Expert Review of Anti-infective Therapy, 2021
Juraj Bosák, Matěj Hrala, Lenka Micenková, David Šmajs
The antibacterial activity of colicins is predominantly directed against E. coli and closely related pathogenic Shigella strains Table 1. Based on the spectrum of activity, colicins can be classified to two groups: (i) colicins with a broad spectrum of activity against E. coli isolates and (ii) colicins with a narrow activity against specific/pathogenic E. coli isolates.