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Anticancer Activity of Bacterial Proteins and Peptides

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Anticancer Activity of Bacterial Proteins and Peptides pharmaceutics Review Anticancer Activity of Bacterial Proteins and Peptides Tomasz M. Karpi ´nski 1,* ID and Artur Adamczak 2 ID 1 Department of Genetics and Pharmaceutical Microbiology, Pozna´nUniversity of Medical Sciences, Swi˛ecickiego4,´ 60-781 Pozna´n,Poland 2 Department of Botany, Breeding and Agricultural Technology of Medicinal Plants, Institute of Natural Fibres and Medicinal Plants, Kolejowa 2, 62-064 Plewiska, Poland; [email protected] * Correspondence: [email protected] or [email protected]; Tel.: +48-61-854-67-20 Received: 23 March 2018; Accepted: 19 April 2018; Published: 30 April 2018 Abstract: Despite much progress in the diagnosis and treatment of cancer, tumour diseases constitute one of the main reasons of deaths worldwide. The side effects of chemotherapy and drug resistance of some cancer types belong to the significant current therapeutic problems. Hence, searching for new anticancer substances and medicines are very important. Among them, bacterial proteins and peptides are a promising group of bioactive compounds and potential anticancer drugs. Some of them, including anticancer antibiotics (actinomycin D, bleomycin, doxorubicin, mitomycin C) and diphtheria toxin, are already used in the cancer treatment, while other substances are in clinical trials (e.g., p28, arginine deiminase ADI) or tested in in vitro research. This review shows the current literature data regarding the anticancer activity of proteins and peptides originated from bacteria: antibiotics, bacteriocins, enzymes, nonribosomal peptides (NRPs), toxins and others such as azurin, p28, Entap and Pep27anal2. The special attention was paid to the still poorly understood active substances obtained from the marine sediment bacteria. In total, 37 chemical compounds or groups of compounds with antitumor properties have been described in the present article. Keywords: anticancer; bacteria; proteins; anticancer antibiotics; anticancer enzymes; nonribosomal peptides; bacteriocins; bacterial toxins 1. Introduction Cancer belongs to the main reasons of morbidity and mortality in the world. In the year 2012, approximately 14 million new cancer cases were detected [1]. In 2015, cancer was responsible for 8.8 million deaths. Lung, liver, colorectal, stomach and breast cancers were the most common causes of death [2,3]. To reduce premature mortality from cancer, the resolution: ‘Cancer Prevention and Control in the Context of an Integrated Approach’ (WHA70.12) was passed in 2017 by the World Health Assembly [4]. Cancerous cells are altered host cells without the natural mechanisms controlling their normal growth. Oncogenesis can be caused by environmentally induced or inherited genetic mutations. It leads to inhibition of cell reaction to the control mechanisms of normal growth and gives rise to the rapid development of cell clones producing neoplasm [5]. Treatment of cancer involves apoptosis induction and tumour-cell proliferation inhibition [6]. According to Hanahan and Weinberg [7], cancer cells exhibit six important changes in their own physiology: (1) self-sufficiency in signals of growth, (2) insensitivity to signals inhibiting growth, (3) resistance to apoptosis, (4) unlimited proliferative potential, (5) sustained angiogenesis and (6) metastasis. One of the available treatments for cancer is chemotherapy, which very often belongs to the main choice of treatment. Unfortunately, chemotherapy can lead to damage of healthy cells and tissues or development of drug resistance [8]. Pharmaceutics 2018, 10, 54; doi:10.3390/pharmaceutics10020054 www.mdpi.com/journal/pharmaceutics PharmaceuticsPharmaceutics 2018,2018 10, 10, x, 54FOR PEER REVIEW 2 of2 26of 26 The most known examples of usage of bacteria and their metabolites for the cancer treatment The most known examples of usage of bacteria and their metabolites for the cancer treatment are are investigations made by William Coley [9], who utilized Streptococcus pyogenes and Serratia investigations made by William Coley [9], who utilized Streptococcus pyogenes and Serratia marcescens marcescenssupernatants supernatants in the treatment in the treatment of patients of with patients unresectable with unresectable tumours. This tumours mixture,. This called mixture today, called as today‘Coley’s as ‘ toxins’,Coley’s wastoxins used’, inwas approximately used in approximat 1200 patientsely 1200 with patients malignancy. with Cancer malignancy. regression Cancer in regression52 cases, includingin 52 cases complete, including cure complete of 30 patients, cure was of 30 observed. patients Mechanism, was observed of this. Mechanism reaction has nowof this reactionbeen partially has now recognized. been partially Microbial recognized. infections canMicrobial activate macrophagesinfections can and activat lymphocytese macrophages and induce and lymphocytesthe cytotoxic and substance induce production,the cytotoxic particularly substance tumourproduction, necrosis particularly factor α (TNF- tumourα)[ necrosis10]. Currently, factor α (TNFbacterial-α) [10 proteins]. Currently, and peptides bacterial are proteins important and as peptides antiproliferative are important agents. Someas antiproliferative of these are already agents. Someused of in these cancer are treatment, already used others in arecancer in human treatment, clinical others trials are or studiedin humanin vitroclinical. In trials this paper, or studied main in vitroanticancer. In this proteins paper, and main peptides anticanc of bacterialer proteins origin and are presented.peptides Suggestedof bacterial division origin of theare describedpresented. Suggestedproteins anddivision peptides of the is showndescribed in Figure proteins1. and peptides is shown in Figure 1. FigureFigure 1. 1. DivisionDivision of of the the described described anticancer proteinsproteins and and peptides. peptides. 2. 2.Antibiotics Antibiotics AccordingAccording to to EncyclopaediaEncyclopaedia Br Britannicaitannica [1[111]],, antibioticsantibiotics areare thethe chemical chemical compounds compounds produced produced mostlymostly by by the the microorganismsmicroorganism ands and injurious injurious to other to other organisms organisms from this from group. this It hasgroup been. I observedt has been observedthat some that of some the antibiotics of the antibiotics also have also anticancer have anticancer activity and activity recently and they recently have been they used have mainly been used as mainlyantitumor as antitumor drugs. The drugs. origin The and origin biological and targetbiological of four target antibiotics of four already antibiotics utilized already in medicine utilized as in medicinechemotherapeutic as chemotherapeutic drugs are presented drugs are in presented Table1 and in theirTable chemical 1 and their structures chemical in Figurestructure2. s in Figure 2. Pharmaceutics 2018, 10, x FOR PEER REVIEW 3 of 26 Table 1. The origin and biological activity of anticancer antibiotics. Biological Target: No. Protein/Peptide Source IC50 References Human Cancer Cells Pharmaceutics 2018, 10, 54 Wilms cancer, Ewing sarcoma, 3 of 26 Actinomyces from 0.4 nM 1 Actinomycin D neuroblastomas, trophoblastic [12–15] antibioticus to 0.42 µM tumours Table 1. The origin andhead biological and neck activity squamous of anticancer cell antibiotics. carcinomas, Hodgkin’s disease, Streptomyces Biological Target: from 25.2 nM 2 No. Protein/PeptideBleomycin Source non-Hodgkin’s lymphoma, testicular IC References[12,16–19] verticillus Human Cancer Cells to 2.93 50mM carcinomas, ovarian cancer, malignant Actinomyces Wilms cancer, Ewing sarcoma, neuroblastomas, from 0.4 nM to 1 Actinomycin D pleural effusion [12–15] antibioticus trophoblastic tumours 0.42 µM acute lymphoblastic leukaemia, acute head and neck squamous cell carcinomas, myeloblastic leukaemia, Wilms’ Streptomyces Hodgkin’s disease, non-Hodgkin’s lymphoma, from 25.2 nM to 2 Bleomycin [12,16–19] verticillus tumourtesticular, neuroblastoma, carcinomas, ovarian soft cancer,tissue 2.93 mM Streptomyces and bonemalignant sarcomas, pleural breast effusion carcinoma, from 548.2 nM 3 Doxorubicin peucetius var. ovarianacute lymphoblastic carcinoma, transitional leukaemia, acute cell [12,20–23] to 44.7 µM caesius bladdermyeloblastic carcinoma, leukaemia, thyroid Wilms’ carcinoma, tumour, neuroblastoma, soft tissue and bone sarcomas, Streptomyces gastric carcinoma, Hodgkin’s disease, breast carcinoma, ovarian carcinoma, from 548.2 nM 3 Doxorubicin peucetius var. [12,20–23] maltransitionalignant celllymphoma, bladder carcinoma, bronchogenic thyroid to 44.7 µM caesius carcinoma,carcinoma, gastricoral squamous carcinoma, carcinoma Hodgkin’s disease,cancers malignant of the head lymphoma, and neck, bronchogenic lungs, carcinoma, oral squamous carcinoma breast, cervix, bladder, colorectal and Streptomyces from 9.48 nM 4 Mitomycin C cancersanal of carcinomas, the head and neck,hepatic lungs, cell breast, [12,24–26] Streptomyces cervix, bladder, colorectal and anal carcinomas, from 9.48 nM to 4 Mitomycin C caespitosus to 249 µM [12,24–26] caespitosus hepaticcarcinom cella, carcinoma, melanoma, melanoma, stomach stomach and 249 µM pancreaticand pancreatic carcinomas carcinomas ICIC50—50—halfhalf maximal maximal inhibitory concentration. concentration. (a) (b) (c) (d) Figure 2.2. ChemicalChemical structures structures of of anticancer anticancer antibiotics antibiotics:: (a) (aActinomycin) Actinomycin D; D;(b) (Bleomycinb) Bleomycin A2; A2;(c) (Doxoc) Doxorubicin;rubicin; (d) (Mitomycind) Mitomycin C. C. 2.1. Actinomycin
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