Studies encompassing the last two decades have shown overwhelming evidences that infection of sexually-transmitted human papillomavirus HPV is connected with the growth cervical cancer 10 , Nevertheless various studies have demonstrated that C trachomatis infection is also linked with the growth and development of cervical cancer Seven diverse viruses have been connected to the growth of different types of human cancer, such as human papillomavirus, Epstein-Barr virus, human T-cell lymphotropic virus, hepatitis B virus, hepatitis C virus, Merkel cell polyomavirus and Kaposi's sarcoma herpes virus.
Although infection of human papilloma virus HPV is considered one of the most essential factor for the growth of cervical cancer 19 but various other factors also connected for the development of cervical cancer which include infection of C. Though, the infection of HPV is generally transient but little percentage of females showed persistent infection which has connected with the development of cervical cancer. Different strains of HPV play important role in the progression and development of cervical cancer.
Every HPV genotype proceeds as an independent infection, with different level of carcinogenesis. Most of the persons are infected with the infection of HPV soon after the beginning of sexual activity as the virus has the potential of transmission by sexual contact.
These causes include physical stress, immune response and other sexually transmitted bacterial infections. The bacterial infection may act as a powerful co-factor for the transformation in host cell for the progression of cervical cancer.
The infection of sexually transmitted bacterium C. It is demonstrated that C. Moreover, C. In general, the growth and development of cancer is a complex multistep procedure, which is also factual for bacterial mediated progression of cancer. The specific pathogenic strains of different types of bacteria exert enigmatic effects on various pathways of host cell 6 , 7 , 15 , Bacteria may alter the normal functions of host cells using different strategies including mutations, altered regulations of various biochemical pathways, cell proliferation, apoptosis which are connected with the initiation and growth of cancer.
In the last decade, many reports have shown the role of C. One of the most prominent attribute is faulty homologous recombination HR repair. Although, the mechanism of these mutational processes is not well understood, and therefore it is fascinating to know that the infection of obligate intracellular bacterium C.
A study showed that infection of C. DSBs demonstrate the most dangerous form of DNA damage due to their unrepaired nature in general and therefore it may cause the risk of instability in the genome of organism DNA damage response DDR delays the genomic instability and increase the frequency of mutations 31 , In our recent studies, we have illustrated the potential involvement of bacterial proteins in the growth and development of different types of cancer through alteration in normal functioning of different pathways 6 , 7 , The host cells protected from cell death-inducing stimuli during the infection of C.
A recent study discloses that plasmid-encoded protein Pgp3 of C. Pgp3 has the potential to stimulate the infected cell for the formation of pro-inflammatory cytokines through Toll-like receptor 2 TLR2 signaling pathway and activation of NALP3 inflammasome which suggest that the Pgp3 of C.
Various proteins of C. Chlamydia is another bacterial genus which is also proposed to be involved in cancer. However, contradictory evidences exist, but the implication of C. Although exact role of Chlamydia in the carcinogenesis is still a subject of discussion, the occurrence of nucleomodulins in these organisms supports their role in the etiology of cervical cancer. Chlamydia has the ability to alter the chromatin structure due to the presences of SET domain proteins.
The implication of SET domain proteins in the etiology of cancer has reported previously 40 , which has showed that some SET domain proteins detected in Chlamydia with the capability to modify chromatin of host. Moreover, Chlamydia is identified to contain various other proteins with the potential to target the nucleus of host during infection. There are several other proteins of Chlamydia with no known potential function are discovered to localize in host cell nucleus.
Perhaps the upcoming advanced research will reveal the enigmatic role of Chlamydia in the growth and development of cancer with molecular study of nucleomodulins. The 3 rd most common cervical cancer is considered as the 4 th leading source of cancer death globally in females.
Although various factors are connected with the growth of cervical cancer, the infection of Chlamydia is also proposed for growth and development of cancer. Different proteins of C. Bacteria have the potential to alter the different regulatory molecules of infected cell during infection for their survival. Various bacterial proteins can modify the normal pattern of gene expression and normal functions of different proteins and enzymes of infected cell through the disturbance in various protein-protein interactions, program cell death, cytoskeletal rearrangement etc.
The obligate gram-negative intracellular pathogen C. Earlier studies have been showed that the infection of C. It has been observed that C. This advocates that the infection of C. Therefore, we may suggest that some proteins of C. Various sub-cellular targeted proteins can exert adverse effects which may inhibit various essential biological functions and responsible for the growth and development of cancer It has observed that the infection of Chlamydia on cultured cells causes multinucleation which directs the chromosomal instability Multinucleated cells are commonly found in most of the solid tumors which contribute in the condition of aneuploidy and chromosome instability Recent report showed that C.
DNA binding proteins have crucial role in the growth and development of cancer. For instance, various DNA binding proteins such as CpG binding proteins triggers the growth of cancer by the process of methylation Similarly chromodomain helicase DNA binding protein 5 is associated with tumour suppression, and mutation in this protein inhibits its function and enhance the growth of breast cancer The existence of DNA binding proteins of human and C. This competitive environment may affect the binding of normal human proteins and increase the risk of cervical cancer.
The normal functioning of different pathways of C. Alteration in normal functions of different pathways of C. Implication of DNA binding inhibitor proteins in growth and progression of cancer has been confirmed in ovarian cancer, where over expression of inhibitor of DNA binding protein ID-1 directs the growth of ovarian cancer These DNA binding proteins may be involved in the growth of cervical cancer and must be investigated further. This mechanism directs double stand brakes and helps to generate senescence-mediated heterochromatin foci.
Chumduri et al, showed that the infection of C. The cells infected with C. Moreover, many DNA damaging endonucleases are also observed which are associated to the growth of cancer, such as primary gastric cancer and lymph node metastasis is associated with the overexpression of LINE-1 endonuclease 55 , As illustrated in above paragraph, the host DNA damage occurrs in C.
We have predicted of C. Nevertheless the prediction results required the validation through wet lab experiments and their implication the growth of cervical cancer. The error recognition and following activation of the DNA damage repair mechanism depends on the complex of the enzymatic proteins which includes MuH MutS, and MutL The MutS complex has the capability to identify mismatched nucleotides and attach to the damaged DNA. Alteration in DNA mismatch repair proteins may direct microsatellite instability, a general event of progression and development of cancer 58 , For instance, mismatch DNA repair protein MutS is associated with the growth of colon cancer 24 , We have also predicted the nuclear targeting potential in C.
It has previously proposed that C. The upcoming advanced research on the role of nuclear targeted C. The infection of sexually transmitted C. Further, the infection of C. Gonzalez et al. Moreover the bacteria Chlamydia have the potential to exploiting the functional interdependence between cell survival and metabolic pathways 30 , Various types of cancers have demonstrated with this process, where activation of oncogenes or loss of tumor suppressors helps to direct the metabolic reprogramming through increased glycolysis and nutrient uptake.
Similar to other gram-negative bacterial strains, C. These effectors proteins prompt bacterial uptake, survival and replication within the host cell. It has observed that glycogen synthase GlgA of C. In fact, GlgA secretion into the inclusion lumen and cytoplasm of host cell has been confirmed The synthesis of glycogen is stimulated in hypoxia stage through the hypoxia-inducible factor which helps in the survival of cancer cell.
Cancer micro-environments have the potential to alter the functions of the different immune cells as per requirement. In immune-elimination state, active cells of immune system eradicate transformed cells. However, during the establishment of cancer, the cells of innate and adaptive immunity provide protection to transformed cells and help for the fulfillment of their requirement.
In between the state of elimination and establishment, equilibrium and escaping state control the response of immune cells. Epidemiological associations indicate that C. It is showed that C. Reports demonstrated that the existence of antibodies to C. Although various cohort studies showed that infection of HPV is connected with the growth of cervical cancer, but it is also observed that the infection of C.
The bacterial infection acts as a potential factor to alter the normal functioning of host cell through various strategies. The infected host cells activate different defensives pathways against to pathogenic infection.
The intracellular infection of bacterium C. Indeed, multiplication of C. A probable molecular mechanism in growth of cervical cancer is the infection-associated inflammatory response during the infection of C. On the other hand during the infection of C. These alterations can cause damages to DNA and impair the function of DNA repair which may increase the genetic instability The C.
Additionally, the infection of C. Similarly it was revealed that infection of C. Immunogenic responses act as a possible factor for the growth of cervical cancer Fig. Abnormal immunogenic responses help in growth and development of cervical cancer during C. It is connected with ectopic condition of pregnancy, pelvic inflammation, and sterility in various cases, and is also involved to enhance the possibility of cervical neoplasia with slow growth cycle The infection of C.
Defensive immune responses manage the bacterial infection while pathological reactions direct to chronic inflammations The process of carcinogenesis has triggered by different factors and events. Bacterial infection may promote the chronic inflammation, which acts as an important factor for the growth of cancer. First line of host defense is provided by the mucosal epithelium of the genital tract.
The innate immunity is triggered while the C. Although C. The role of such cytokines have been observed in the growth and development of cancer, invasion and metastasis Moreover, chemokines including IL-8 can enhance recruitment of innate-immune response control cells including dendritic cells DCs , natural killer NK cells, macrophages, and neutrophils that consecutively generate more proinflammatory cytokines to restrict the growth of C.
Matrix metalloproteases MMPs is released by the infected mucosal epithelial cells which contribute in tissue proteolysis and remodeling. Neutrophils also release MMPs and elastases that contribute to tissue damage.
DCs play important role in processing and presenting of C. A study showed that depletion in CD4 cells, are not capable to eliminate the infection of C. Nevertheless, another report demonstrated that transfer of Chlamydia specific monoclonal antibodies into B-cell deficient and CD4 depleted cells re-established the capability of these mice to control a secondary infection of C.
This phenomenon shows a powerful synergy between CD4 and B cells in the adaptive immune response to C. In contrast, the CD8 cells of immune system generate various interleukins such as IL-4, IL-5, and IL- 13 which do not emerge to defend against Chlamydia infection and may even indirectly increase the load of Chlamydia through inhibiting the protective response of CD4.
This outcome proposes that a biased immune response toward Th1 occurrence defends against the chronic infection The pathogenic response to C. On the other hand, chronic infection can arise if the response of Th2 dominates on the Th1 immune response and consequence activate the autoimmunity and cell damage which has triggered the tissue inflammation.
This Inflammation enhances the heat shock protein HSP expression in host, which stimulate IL production through auto-antibodies during the course of C. It has demonstrated that the cells of cervical epithelium express an efficient inflammasome which directs to activation of caspase-1 by a procedure involving the NOD-like receptor family member NLRP3 along with inflammasome adaptor protein during C. Therefore, it is required to expand the screening of C.
This strategy will help to prevent cervical cancer. In conclusion, the current systematic review illustrate that the women infected with infection of C. These include alteration in the normal functioning of different pathways such as apoptosis, DNA repair system, protein folding during the infection of C. Different processes are involved in growth and development of malignancy during host pathogen interactions. The mechanism of C. Host pathogen interaction is a very complex mechanism involving a range of molecules such as nucleomodulins.
Nucleus is an important sub-cellular organelle of the cell and has key role in oncogenesis. Controlling of this cell organelle by pathogen is a crucial phenomenon and must be considered to understand the implications of bacteria in carcinogenesis.
Though, various techniques are available to identify nuclear targeting of certain protein and its consequent effects on the functions of nucleus, but it is very difficult to evaluate complete bacterial proteome for their nucleomodulins potential.
Several in-silico approaches are also accessible to balance this problem through deciphering the nuclear targeting of certain proteins rapidly. The present research indicates that certain specific proteins of C. National Center for Biotechnology Information , U.
Journal List J Cancer v. J Cancer. Published online Jun Find articles by Xingju Yang. Find articles by Anam Siddique. Find articles by Abdul Arif Khan. Find articles by Qian Wang. Find articles by Abdul Malik. Find articles by Arif Tasleem Jan. Find articles by Hassan Ahmed Rudayni. Find articles by Anis Ahmad Chaudhary. Find articles by Shahanavaj Khan. Author information Article notes Copyright and License information Disclaimer.
Shahanavaj Khan, E-mail: as. Department of Pharmaceutics, College of Pharmacy, P. Competing Interests: The authors have declared that no competing interest exists. Received Jan 23; Accepted May Abstract Pathogenic bacterial strains can alter the normal function of cells and induce different levels of inflammatory responses that are connected to the development of different diseases, such as tuberculosis, diarrhea, cancer etc.
Keywords: bacteria, C. Introduction Cancer is very complex and deadly disease worldwide. Role of infections in the etiology of cervical cancer Infections of various microorganism including viruses, parasites and bacteria, have been categorized as possible risk factors for the progression and development of different type of cancers. Bacterial infection and cervical cancer In the last decade, many reports have shown the role of C. Chlamydia infection and risk of cancer Chlamydia is another bacterial genus which is also proposed to be involved in cancer.
Chlamydia trachomatis and cervical cancer The 3 rd most common cervical cancer is considered as the 4 th leading source of cancer death globally in females. Possible implications of C. Possible erroneous in DNA binding proteins and cervical cancer DNA binding proteins have crucial role in the growth and development of cancer. Open in a separate window. Figure 1. Possible alteration in the DNA damage proteins and cervical cancer C.
Inhibition in apoptosis during infection of C. Delivery of C. Inflammation in carcinogenesis of cervical cancer Cancer micro-environments have the potential to alter the functions of the different immune cells as per requirement. Infection mediated immune response and cancer The bacterial infection acts as a potential factor to alter the normal functioning of host cell through various strategies. That is the most famous characteristic. So that's our answer here. The spirit carries the.
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