Hypothesis Cancerogenic Hypercycle: a New Conception of Cancer Treatment

Home , Hypercycle (chemistry)

2013 Sep 01;1(2):12. 2013 Sep 01;1(2):12. citationFor purposes: 30159 Hanover, Germany Department Practice ofUrologie, Bahnhofstr 1, Email: * Corresponding author catalyst for their processing was reactions, i.e.reactions in which the tion were autocatalytic chemical primary forms oflife self-organiza the states of evolutionalchemistry, bytion DNA replication.According to the transmission of genetic informa structureschical cell which ensured replicationforms to complex hierar direction from thesimplestRNA oped by self-organizing inthe Evolutionallife onearthhasdevel Introduction and treatment. elaboratemethods of itscontrol new allowwill to detect cancer early, to Computerof thisprocess modelling Conclusion this hypothesis. confirm data biology molecular The Evaluation ofhypothesis subject to computer modelling. on laws of synergetic andcanbe worlds. This process develops based competition oftheDNA andtheRNA generated by disintegration and cell self-organization outof the chaos the creationformnew ofa of inner- hypercycle explains thisprocess by The hypothesis onthecancerous The hypothesis cancerogenic hypercycle treatment. clones. This cell paper discusses process of creation of new cancerous cancerous progression, explainesis cannot the process of Modern theories onthecarcinogen Introduction Abstract Medicine [email protected] Licensee OA Publishing London2013.Creative Commons Attribution License(CC-BY) VN Malzev* Cancerogenic hypercycle:anewconceptionof Malzev VN. i.e. the Cancerogenic hypercycle: a new conception of cancer treatment. OA Medical Hypothesis Hypothesis Medical OA treatment. cancer of conception new a hypercycle:Cancerogenic - - - - -

hence merge two cyclicreactions ina byreactions. both These enzymes reaction,i.e. suchenzymes are shared the oneaswell asoftheothercyclic which areto able replicate theRNA of coding by these RNA’s of enzymes their merginghypercycle ina isthe cyclic RNA replicationreactions and for competition and cooperation of two reasons the of One (pр.18–29). systemstable of evolution capable of self-reproducing unitsinanew merging of means a is This one. first reaction produces catalysts for the lysts of theother one, andthelast by-products of one reaction are cata tions organized in the way that A hypercycle is several cyclic reac closed autocatalytic chemicalcycles. reproducing macromolecules in hypercyclemeans ofmerging isa self- tures, referred to ashypercycles. A and generate more complex struc enter in interactions witheach other catalytic reactions are alreadyto able to beperformed by RNA. These auto genetic information carrier remained of catalysts–enzymes, and therole of specialized proteins took ontherole tion ofbiochemicalreactions, developmenttional specializa and was notrequired from theoutside. reactions themselves, and for which it generated intheprocess of these u hptei cnit o the of consists mechanism of the that, assumption hypothesis Our The hypothesis cycle”. interference asacancerous hyper showwill below in thesection “RNA and inRNA interference, which we cancerous hypercycle development playanism can roleimportant an in hypercycle In the processIn of furtherevolu cancer treatment 1 (pр.218–219). This mech ------1

life formAn example in thecell. for basis fora as more a highly developed cycle have notdisappeared and serve which serve asthebaseforhyper a in which they were performed. committees related to theinstitution approved by therelevantethics protocols ofthesestudieshave been ownstudies inthishypothesis. The The author has referenced some of its Evaluation ofthehypothesis cancer creation. hypercycles creationis thebasisof ogenic nature of such ahypercycle cancerogenic hypercycle. The cancer world, suchahypercycle becomes a progress which displaces theDNA of such amerging is RNA world hypercycle is generated. If the result a later), examined is and separately fermentative mechanism stands or byunit RNAinterference (this one aswellas ontheotherreplicative enzymes which produceon impact each other by meansofshared simple replicativemerge units with each otherbymembrane. a If these from separated replication) RNA and replicative units(DNA replication (subsequently: “DNA world”). translationand tion processes ized proteins generated by transcrip DNA replication is played by special DNA, andtherole ofthecatalyst for information carrier is played by the world inwhich the role of the genetic RNA replication forms asRNA world. subsequently refer to these simplest bacterial cell replicationis phage enhancing in a such a cyclic reaction withauto- CyclicRNA replication reactions A DNA world is asystem ofsimple A developed life form includes a To simplifytheexplanation,we 1 (pр.26–27).

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Competing interests: none declared. Conflict of interests: none declared. All authors contributed to conception and design, manuscript preparation, read and approved the final manuscript. All authors abide by the Association for Medical Ethics (AME) ethical rules of disclosure. Page of 6

2 Hypothesis

can be explained by the fact that RNA process when a more highly organ- cancerogenesis are regarded by us as replication is a much more mutagenic ized form of matter is replaced by a a secondary process. process than DNA replication. This less organized form. This replacing Some authors of the epigenetic mutagenic process spreads on the and displacing takes place by the theory of cancer generation claim DNA world by epigenetic reprogram- mutagenic impact of one of the that DNA perturbation in the cell ming of DNA, i.e. by DNA methylation. components of the RNA world– nucleus takes place under the impact The creation of a hypercycle of an “epigenetic code5“, but do not and/or of the mutating RNA itself, by explain the origin of this epigenetic based on shared enzymes, can only theenzyme mechanism which fulfils of RNA the interference replication, code. The newness of our hypothesis takeaccording place toin the the first absence characteristic, of a nuclear i.e. which is considered below. The muta- is the explanation of the origin of this membrane, which is the case during a genic impact expressed in DNA meth- “code“ as a cancerous hypercycle cell division cycle or when the ylation entails epigenetic DNA code able to generate and develop membrane is damaged. For a cancerous reprogramming in such a way that autonomously and spontaneously in tumour, generation of pathological the genes which enhance the RNA the cell. forms and prolonging of the mitosis world are subject to expression. Path- The questions how and why the metaphase is characteristic . ological DNA methylation and the processes of DNA world cooperation This is why the time of absence2 of a displacing of the DNA world by the and generation of primary life forms cell membrane in the mitosis process RNA world as a result of competition are replaced by competition in a cancerous cell increases in for energetic cell resources, whose processes were discussed in our comparison to such a time in a normal lack entails the limitation of the precedent work6. cell, and the forming of a cancero- possibility for the DNA world to self- genic hypercycle is facilitated. restore, entails genetic instability and a cancerous cell, as well as any life Examples of a hypercyclic link generation of DNA mutations. As a form,Here, is awe dissipative would just system like to fromadd that the based on shared ferments are consid- result of this process, the DNA world synergetic point of view . The differ- ered in the chapter “shared ferments gains characteristics which are innate ence of a dissipative system7 of a as a kind of hypercyclic link of a to the RNA world–mutagenesis char- cancerous cell from a dissipative cancerous hypercycle”. acter and a progressing development The creation of a hypercycle with generation of new cell clones, organization of a new order based on according to the second character- which is, in essence, generation of RNAsystem world of a normalprogress, cell and, is, firstly,secondly, the istic, i.e. by RNA interference, takes new life species. the higher degree of entropy as a place in the presence of a nuclear Some authors have already come to measurement of chaos, i.e. freedom membrane. No conditions of the view of cancer as a new form variations for individual units of this membrane absence or damage are 3,4. system. This is expressed in cell required. RNA interference is also a Therefore, the cancerogenesis anaplasia, in expression of genes not fermentative mechanism which is process(species) is regarded by us not as a innate to a normal cell, in the fact that shared by two simple cyclic units. An unique incident in the kind of one or organelles of a cancerous cell stop to example of a hypercyclic link based several DNA mutations, but as a on RNA interference is presented in process of continuous incidents of them: mitochondria stop to supply the chapter “RNA interference as a thefulfil thecell functions via aerobic normally glycolysis, innate to form of hypercyclic link of a cancerous whose uninterrupted nature and lysosomes stop to participate in hypercycle”. continuousnessepigenetic modifications is ensured in the by DNA, the apoptosis. This is expressed i.e. in the RNA world progress and spreading, relative autonomization of the RNA RNA world, remaining in the cell and and which is referred to as hyper- world as a result of perturbation of integratedOur hypothesis in inner assumes cell processes, that the cycle. The involving of cell structures links between elements of the DNA begins to play the leading role in in it, as well as the involving of the world. cancerogenesis as a result of disinte- nuclear DNA itself, is referred to as The generation of cancer as a new gration and competing interaction cancerogenic hypercycle. form of a dissipative system is subject with the DNA world by its ability of to synergetic laws. Due to the chaos self-organization and autonomous group of epigenetic hypotheses of generated as a result of perturbation evolution after the loss of control cancerOur generation hypothesis as belongs cancer genera to the- of the DNA world control over the over it by the DNA world. Resulting tion is explained by it with processes RNA world and competition of two from this competition, replacing and which take place not in the nuclear systems, here the DNA and RNA displacing of the DNA world by the DNA, but in the cell cytoplasm. DNA worlds, resulting from a coincident RNA world takes place, a degradation mutations which take place in

fluctuation whose role can be played

Licensee OA Publishing London 2013. Creative Commons Attribution License (CC-BY) Malzev VN. Competing interests: none declared. Conflict of interests: none declared. interests: none declared. Conflict of interests: Competing the final manuscript. preparation, read and approved and design, manuscript conception to All authors contributed rules of disclosure. ethical Ethics (AME) for Medical the Association All authors abide by For citation purposes: Cancerogenic hypercycle: a new conception of cancer treatment. OA Medical Hypothesis 2013 Sep 01;1(2):12. Page 3 of 6

Hypothesis

by cancerogenic factors, by a Thom relatively simple to evaluate a hyper- reprogramming only, in this case, catastrophe, and having bypassed the cycle composed of two cyclic reactions damage of the DNA world also takes bifurcation point, an irreversible in which the ferment of one cyclic reac- place due to competition for ener- state of a new balance is created, i.e. a tion can cause RNA replication of the getic cell resources and, as a conse- new dissipative system in which other cyclic reaction, and the ferment quence, limited self-restoration there will be different order parame- of the second cyclic reaction can only possibility of the DNA world. ters than in the dissipative DNA world cause the replication of its own RNA system. The generation of such a new and cannot replicate the RNA of the RNA interference as a form of a dissipative system is probable and hypercyclic link of a cancerous not predetermined. the hypercycle promote the replication hypercycle Laws of synergetic determine offirst one cyclic of two reaction. RNAs more, If both the ferments winner ofin To understand the development mech- cancer diagnostic and treatment, the competition of these two cyclic anism of a cancerogenic hypercycle via which is scrutinized below. reactions will be this particular RNA RNA interference, it is necessary to replication reaction1 stop shortly at how RNA interference Empirical Data case of a hypercycle with two cyclic functions in a normal cell. Shared ferments as a kind of reactions–in our case, (р.219).i.e. cyclic InsiRNA the Normally, the transcription and hypercyclic link of a cancerous replication reaction and iRNA replica- translation regulation runs in the way hypercycle tion–the winner of the competition of pre-miRNA–interaction with dsRNA can be a cyclic reaction which will be siRNA, i.e. the RNA world, as Dicer–interaction with RNA-induced serves as the base for a cancerogenic RdRP replicates only the siRNA, but hypercycle created by RNA interfer- cannot replicate iRNA. Yet, the DNA- “epigenetic code” of a normal cell is ence, and any ferment able to cause dependent RNA polymerase II can silencing complex (RISC). Hence, the RNA-dependent RNA replication can Pre-miRNA as well as dsRNA be the enzyme. Such an enzymatic in sum, these two ferments promote interactrealized (Figurewith the 1). same structures in activity is possessed by RNA- siRNAreplicate than iRNA iRNA as more.well as siRNA. Hence, the cell cytoplasm–with the protein , If a third cyclic reaction joins the complex Dicer and the RISC complex, DNA-dependent RNA polymerase II, hypercycle, in our case a revertase whose central element is endonu- retroviraldependent RNAreverse polymerase transcriptases– (RdRP) able to replicate siRNA as well as a clease which belongs to the proteins reverse transcriptase (also known as virus, the advantage of the RNA revertase or RNA-directed DNA poly- world even grows as a third ferment These two classes of short RNAs, merase. (Subsequently: “shared hyper- and is added which enhances siRNA miRNAfamily Argonaute and siRNA, (Ago). are able to . Presence replication. compete for a place in the same effec- 8 torial complexes10, i.e. Dicer and RISC differentcycle enzymes, cyclic abbr.reactions SHE”) is a typical provides a new, different explanation are the shared element which links characteristicof SHE ferments of a ablehypercyclic to catalyse link. of Hence,the viral the theory proposed of cancer hypothesis genera- two cyclic reactions: miRNA replica- Creation of a hypercycle according to tion: cancer is generated resulting tion reaction and dsRNA replication from enhancement of the cancerous reaction, and hence is a form of a above can take place based on such a hypercycle by a cyclic RNA virus hypercyclic link. hypercyclicthe first characteristiclink. This is why mentioned we can replication reaction. A cancerous hypercycle based on regard cyclic reactions of dsRNA repli- The answer to the question RNA interference is created in the replication as whether these ferments can cause, a component of a hypercycle in which - Two elements–Dicer and RISC–are thecation activity and mRNA of these (iRNA) ferments can entail tions of correspondent nucleic acids afollowing place wayof competing (see Figure 2).interaction competition of its components. This innatebesides to specific them, functionsalso DNA of methyla replica- between pre-miRNA and dsRNA particular case deals with merging in a tion, remains open. Yet, such a mech- where competition for replacing the hypercycle of such cyclic reactions as anism is not excluded as cases in the miRNA normally regulating the gene dsRNA replication, iRNA replication nature are known of DNA methyla- transcription and translation by the tion in the absence of methyl trans- cancerogenic dsRNA takes place. cancerous cell has at least three cyclic ferase, which was earlier considered After such a replacing, dsRNA reactionsand DNA able replication. to create a Hence, hypercycle the to be indispensable for methylation . becomes an anti-sense siRNA chain, If a cancerous hypercycle of such9 the latter one methylates and repro- siRNA replication, the second one is form is limited to the process of grams the DNA in the cell nucleus on iRNAvia the replication shared enzymes. reaction, The and first the one third is displacing the DNA world without one is DNA replication reaction. It is methylation and epigenetic DNA normal “epigenetic code”, and the one hand, i.e. it modifies the

Hypothesis

depresses the translation by binding it with the correspondent comple- mentary sequence in the mRNA composition on the other hand. siRNAs are capable of building long

to be primers for synthesis of new RNAsRNA molecules. on a single-stranded Hence, they and/or are able a double-stranded RNA matrix of the RdRP . Prolonging8 siRNA products are double-stranded RNA themselves. This is why they are subject to further

with creation of “secondary” siRNAs andpost-transcriptional a probable participation modification of Dicer.

looks like a degrading polymerase chainHence, reactionthe RNA interferencein which primaryprocess siRNA molecules, being primers for synthesis of new double-stranded RNA molecules, entail creation of secondary siRNAs. Figure 1: Transcription und translation regulation through RNA interference in This process can be autocatalytic, i.e. capable of autonomous evolution, indicated by a dotted line. and correspond to a hypercycle if one a normal cell. Border between DNA world (left) and RNA world (right below) is of the products of this cyclic reaction

- nitelyis SHE as generation. long as RNA is present which is Suchable ato cycle be a can matrix continue for indefisiRNA primers . 8 reaction, as a result of gaining a competingTherefore, advantage the cyclic over dsRNA-SHE the cyclic translation miRNA-mRNA degradation control reaction, the RNA interference mechanism displaces and replaces the latter one. Reasons for generation of a competing advantage of the RNA world over the DNA world were indicated in our precedent work6 expressed in decrease of miRNA concentration. On a molecular and increase level, of thissiRNA is concentration.

Consequences of hypothesis In the case of the creation of a cancerous hypercycle by RNA interference, siRNA increase at the back- Figure 2: ground of miRNA decrease takes through RNA interference in a cancerous cell. Border between DNA world (left Spreading of the carcinogenic hypercycle (Rd-dsRNA) on translation of our hypothesis. Some facts place. Such a profile speaks in favour below) and RNA world (right) is indicated by a dotted line.

Hypothesis

structure. As our hypothesis assumes corresponds in a great measure to the incidents in a cancerous cell are the generation of a new system from DNA methylation image of the human alreadyconfirming proven. such a development of the elements of the precedent system, bowel cancer, it is to be expected that Such facts include high dsRNA the proving of the hypothesis the cancerogenic hypercycles struc- mutability and its capability of an requires a synthesis method, a ture determining such a similar autonomous replication, independent computer system modelling method, “epigenetic code” in both cases will of the DNA world. and comparison of this virtual model also be similar14. siRNA, as a dsRNA product, causes to the biological model. For this, a Applying such a method, several cancerogenic effects in a cell . biological model should be chosen– goals at one time can be achieved. The capability of competition11,12 for an animal with a certain cancer form, The existence of a cancerous hyper- the epigenetic regulation of tran- the miRNA and siRNA concentrations cycle can be proven as well as new scription and translation between the in it as well as concentration of possibilities for cancer diagnostics, siRNA of a cancerous hypercycle and ferments replicating those RNAs prognosis and treatment can be the miRNA of the DNA world via the should be examined, i.e. the biochem- detected. interference mechanism mentioned above in the section “RNA interfer- Discussion ence as a form of a hypercyclic link of comparedical profile ofto RNA the and correspondent enzymes is to New conception of cancer a cancerogenic hypercycle” is also be examined. This profile should be treatment animals. Based on the evaluated Acting on the assumption of the The fact of miRNA depression in a differences,profile of the controla groupmathematical of healthy hypothesis of cancer generation as a confirmed. 13. computer model of a cancerous development of a cancerogenic Therefore, there are at present hypercycle can be constructed and hypercycle, we have to look differ- enoughcancerous facts cell indicating is also confirmed a competing virtual experiments can be ently at the impact mechanism of interaction between siRNA–RdRP conducted, depressing the activity of known anti-tumour treatment and DNA world for the epigenetic such or such enzymes of the hyper- methods as well as on the cancer control over the transcription and cycle or modifying in a certain way diagnostics and treatment strategy. translation in a cell, and also indi- other parameters of cyclic reactions The task of diagnostics becomes to cating the fact that this control is, in a detect the order parameters of the cancerous cell, under the regulation agents participating in the reaction new dissipative system which the of a new RNA world order organizer (pH, concentration of chemical cancerous cell is. Such parameters represented by the siRNA–RdRP that there is already experience of are, most probably, siRNA, miRNA hypercycle. The quoted facts also mathematicaland other). It modelling should be of mentioned hypercy- indicate the displacing and replacing cles1 The task of treatment becomes the of miRNA by the product of the creationand SHE ofactivity. conditions in the cell that cancerous siRNA hypercycle, i.e. on a(pр.80–175). cancerogenic Hence, hypercycle it can beto would change the competing interac- displacing and replacing of the DNA createclarified a whichThom impactcatastrophe must withbe made the tion between the DNA world and the world by the RNA world. goal to create a new dissipative RNA world to a competing advantage The quoted facts are in favour of system in which the DNA world in favour of the DNA world. This is the our hypothesis, but they cannot serve would gain a selective advantage and newness of the proposed cancer prevail over the RNA world, and the treatment conception and its differ- our hypothesis cannot be proven generation probability of this new ence from the modern cancer basedas its definiteon a biochemical evidence. In analysis general, dissipative system can also be calcu- therapy: radical healing from cancer method, i.e. method of separating a lated. Taking into account the gained is impossible without elimination of whole system to its component result, the same action should be the cancerous hypercycle. elements. A cancerous hypercycle conducted on a real biological model Biochemical reactions run in a rela- can be a quite complex generation and the gained results should be tively narrow interval of physical and including several cyclic reactions compared. The impact control and chemical parameters. To cause a selec- linked to each other by hypercyclic the evaluation of its effectiveness are tive effect with the goal of depressing reactions based on shared ferments conducted by scrutinizing the RNA one reaction and promoting the other as well as on RNA interference. A one, it is necessary to know the differ- simple concentration evaluation of Taking into consideration the fact ence of physical and chemical param- hypercycle components cannot profile and the enzymes. eters of one reaction from those of the provide us an image of the hyper- other one. Applied to our situation, it cycle as a dynamically developing tumours,that the e.g. DNA such methylation as bowel cancer, profile is necessary to know the difference of (“epigenetic code”) in some mice

Hypothesis

RNA replication parameters from the able to cause such an impact is pyro- Alexandrov AA Dr Biol Prof, editor. DNA replication parameters. gallol15. The anti-tumour impact of 8. pyrogallol is already proven16. and“Knowledge realization”. base “RNA of molecular interference: and general RdRP RNA world parameters is the fact that Elaboration of preparations human biology (HUMBIO). Elaboration One such difference in DNA and the mutations number in RNA repli- causing selective depression of Available from: http://humbio.ru/ cancerogenic hypercycle enzymes humbio/rna_interf/00014f46.htmactivity in animals”; “secondarysiRNAs”. mutations number in DNA replica- can be a perspective direction in tion,cation and is significantly when surpassing higher a than certain the cancer treatment. ; http:// threshold of mutations number1 humbio.ru/humbio/rna_interf/00012740. Conclusion “Cytosinehtm, [accessed methylation 15 Aug 2013]. and hydroxymeth- impossible, whereas the DNA world The process of creation of a new clone ylation9. Bracht mark JR, Perlman DNA for DH, eliminationLandweber LF.in is(р.78), capable RNA of self-restoring. replication becomes of cancerous cells is a process of crea- Assuming this, the tactics of radiation of a new dissipative system Oxytricha trifallax”. Genome Biol. 2012 tion cancer treatment also changes. based on creation of a carcinogenic 10. Bellare P, Sontheimer EJ. “A fork in the roadOct;13(10):R99. for microRNAs”. Nat Struct Mol Biol. The treatment task becomes to select hypercycle. This process can be described mathematically and a a radiation dosage that would, on the 11. corresponding model on a computer one hand, not cause too great a loss Baylin2007 Aug;14(8):684–6. JSB. “Short double-stranded RNA for DNA, and on the other hand, can be built. 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