Abstract
There has been increasing evidence that a local inflammatory response stimulates tumor cells to acquire metastatic potential, and the concept of inflammatory oncotaxis has been spreading in recent years. However, the interaction between microbial inflammation and the development of gastrointestinal cancer is still unclear. This review summarizes the present knowledge on the role of microbial inflammation in the development of gastrointestinal cancers from the perspective of molecular biological findings. Chronic inflammation caused by bacterial infection is known to induce cancers as exemplified by Helicobacter pylori, which is associated with the development of gastric cancer via the activation of the TLR4 pathway by bacterial lipopolysaccharide followed by cancer growth through CagA-MET signaling. In addition, the development of inflammatory bowel diseases has been known to become a risk factor for colorectal cancers, where inflammation caused by certain bacterial infections plays a key role. It is also known that the cancer microenvironment is associated with cancer growth. Moreover, infectious complication after surgery for gastrointestinal cancers may promote tumor progression via the stimulation of pathogen-associated molecular patterns and various inflammatory mediators secreted by immunocytes. Further research on the link between microbial inflammation and cancer progression is needed to drive a paradigm shift in cancer treatment.
Highlights
Previous reports suggested that a persistent local inflammatory response stimulated tumor cells to acquire metastatic potential, and the concept of inflammatory oncotaxis has been spreading in recent years [1,2,3,4,5,6]
tumor-associated macrophages (TAMs) produce many bioactive substances such as tissue growth factors, e.g., IL-6, TNFα, angiogenic factors, matrix metalloproteases (MMPs), and immunosuppressive factors, all of which are involved in cancer growth and metastasis
HGF is known to be produced after surgical stress and sepsis [7]. Molecular targeted therapeutics such as anti-EGFR, anti-VEGF, and PD-1/PD-L1 antibodies have been clinically applied in many carcinomas to inhibit angiogenesis and immune checkpoint functions, respectively [8,9,10,11]
Summary
Previous reports suggested that a persistent local inflammatory response stimulated tumor cells to acquire metastatic potential, and the concept of inflammatory oncotaxis has been spreading in recent years [1,2,3,4,5,6]. HGF is known to be produced after surgical stress and sepsis [7]. Molecular targeted therapeutics such as anti-EGFR, anti-VEGF, and PD-1/PD-L1 antibodies have been clinically applied in many carcinomas to inhibit angiogenesis and immune checkpoint functions, respectively [8,9,10,11]. .AAnnoovveerrvvieiewwooffththeelilninkkssbbeetwtweeeennmmicicrorobbiaial lininfefecctitoionn, ,cchhroronnicicininflfalammmmaatitoionn, ,aannddccaanncceerreennvvirioronnmmeennt.t.SSeevveerraall ssigignnaalilninggppaaththwwaayyss, ,ssuucchhaassTTLLRR44aannddCCaaggAA//cc--MMeett,, aanndd mmeeddiiaattoorrsssseelleecctteeddbbyymmiiccrroobbiiaalliinnflflaammmmaattiioonnppllaayyaanniimmppoorrttaanntt rrooleleininththeeddeevveeloloppmmeennttooffggaasstrtrooinintetesstitninaallccaanncceerrss..EEBBVV::EEppsstteeiinn--BBaarrrrvviirruuss;;CCAAFFss:: CCaanncceerr aassssoocciiaatteedd fifibbrroobbllaassttss;; EEMMTT:: EEppiitthheelliiaallmmeesseenncchhyymmaallttrraannssiittiioonn;;HHGGFF::HHeeppaattooccyyttee ggrroowwtthh ffaaccttoorr;; HHPPVV::HHuummaannppaappiilllloommaavviirruuss;;IIFFNN::IInntteerrffeerroonn;;IILLss:: IInntteerrlleeuukkiinnss;;IICCAAMM--11:: IInntteerrcceelllluullaarraaddhheessiioonnmmooleleccuulele-1-1; J;AJAKK/S/TSATTA1T:1Ja: nJaunsuksinkaisnea/sSeig/nSaigl ntraalntsrdanuscderuacnerdaanctdivaacttoivr aotfotrraonftsrcarnispctrioipnti1o;nL1P;SL: LPiSp:oLpioploypsoaclychsaacrcidhea,riMdeM, PMsM: MPas:trMix amtreitxalmloeptraolltoepinraosteesin; aNsFes-κ; βN: Fn-uκcβle: anrufcalcetaorr-fkaacptopra-kβa;pPpAaMβP; sP:APMatPhos:Pgaetnh-oagsesno-caiassteodciamteodlemcuollaercuplaatrtepranttemrnolmecoulleecsu;lResA; RNATNEST:ERSe: gRuelgauteladteodnoancaticvtaivtiaotino,nn, onromrmalalTTcceelllleexxpprreesssseedd aanndd sseeccrreetteedd;; TAMs: Tumor associated macrophages; TGFs: Transforming growth factor; TLR: Toll-like receptor; TNF-α: Tumor necrosis factor-α; VCAM-1: Vascular cell adhesion molecule-1 FFiigguurree11. .AAnnoovveerrvvieiewwooffththeelilninkkssbbeetwtweeeennmmicicrorobbiaial lininfefecctitoionn, ,cchhroronnicicininflfalammmmaatitoionn, ,aannddccaanncceerreennvvirioronnmmeennt.t.SSeevveerraall ssigignnaalilninggppaaththwwaayyss, ,ssuucchhaassTTLLRR44aannddCCaaggAA//cc--MMeett,, aanndd mmeeddiiaattoorrsssseelleecctteeddbbyymmiiccrroobbiiaalliinnflflaammmmaattiioonnppllaayyaanniimmppoorrttaanntt rrooleleininththeeddeevveeloloppmmeennttooffggaasstrtrooinintetesstitninaallccaanncceerrss..EEBBVV::EEppsstteeiinn--BBaarrrrvviirruuss;;CCAAFFss:: CCaanncceerr aassssoocciiaatteedd fifibbrroobbllaassttss;; EEMMTT:: EEppiitthheelliiaallmmeesseenncchhyymmaallttrraannssiittiioonn;;HHGGFF::HHeeppaattooccyyttee ggrroowwtthh ffaaccttoorr;; HHPPVV::HHuummaannppaappiilllloommaavviirruuss;;IIFFNN::IInntteerrffeerroonn;;IILLss:: IInntteerrlleeuukkiinnss;;IICCAAMM--11:: IInntteerrcceelllluullaarraaddhheessiioonnmmooleleccuulele-1-1; J;AJAKK/S/TSATTA1T:1Ja: nJaunsuksinkaisnea/sSeig/nSaigl ntraalntsrdanuscderuacnerdaanctdivaacttoivr aotfotrraonftsrcarnispctrioipnti1o;nL1P;SL: LPiSp:oLpioploypsoaclychsaacrcidhea,riMdeM, PMsM: MPas:trMix amtreitxalmloeptraolltoepinraosteesin; aNsFes-κ; βN: Fn-uκcβle: anrufcalcetaorr-fkaacptopra-kβa;pPpAaMβP; sP:APMatPhos:Pgaetnh-oagsesno-caiassteodciamteodlemcuollaercuplaatrtepranttemrnolmecoulleecsu;lResA; RNATNEST:ERSe: gRuelgauteladteodnoancaticvtaivtiaotino,nn, onromrmalalTTcceelllleexxpprreesssseedd aanndd sseeccrreetteedd;; TAMs: Tumor associated macrophages; TGFs: Transforming growth factor; TLR: Toll-like receptor; TNF-α: Tumor necrosis factor-α; VCAM-1: Vascular cell adhesion molecule-1
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