2015
DOI: 10.1158/0008-5472.can-15-0732
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Stromal Fibroblasts Induce CCL20 through IL6/C/EBPβ to Support the Recruitment of Th17 Cells during Cervical Cancer Progression

Abstract: Cervical cancer is a consequence of persistent infection with human papillomaviruses (HPV). Progression to malignancy is linked to an inflammatory microenvironment comprising T-helper-17 (Th17) cells, a T-cell subset with protumorigenic properties. Neoplastic cells express only low endogenous levels of the Th17 chemoattractant CCL20, and therefore, it is unclear how Th17 cells are recruited to the cervical cancer tissue. In this study, we demonstrate that CCL20 was predominantly expressed in the stroma of cerv… Show more

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Cited by 106 publications
(147 citation statements)
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“…There are reports shown that fibroblasts involve in the cross-talk of cancer cells and fibroblasts by secreting CCL2 [3032], CCL5 [33], CXCL1 [34], CXCL6 [35], CXCL12 [36], IL6 [37], CXCL16 [38] and others [2331]. In the study, we identified that CCL11 and CXCL14 were the target genes of miR-29b in fibroblasts.…”
Section: Discussionmentioning
confidence: 80%
“…There are reports shown that fibroblasts involve in the cross-talk of cancer cells and fibroblasts by secreting CCL2 [3032], CCL5 [33], CXCL1 [34], CXCL6 [35], CXCL12 [36], IL6 [37], CXCL16 [38] and others [2331]. In the study, we identified that CCL11 and CXCL14 were the target genes of miR-29b in fibroblasts.…”
Section: Discussionmentioning
confidence: 80%
“…Moreover, a higher sensitivity was also observed for the topoisomerase II inhibitor etoposide used in recurrent cervical cancer (30), indicating that the sensitization was not restricted to a single class of chemotherapeutic drugs. Although the IL6-/STAT3-pathways appear to be attractive pharmacologic targets to improve the immune microenvironment (9,10,17,18), our data suggest that one should be cautious to combine STAT3 inhibitors with cisplatin or etoposide in cervical cancer patients.…”
Section: Discussionmentioning
confidence: 88%
“…IL6 has a negative impact on the prognosis of a patient (16). We have shown that it mainly acts in a paracrine manner and creates a protumorigenic and immunosuppressive microenvironment (10,17,18). Cervical cancer cells display only low responses to autocrine IL6 due to low gp80 expression levels (15,19) but sgp80 can restore autocrine IL6 signaling and induce pronounced STAT3-binding activity (15).…”
Section: Introductionmentioning
confidence: 99%
“…There is a strong need for new therapeutic strategies in cervical cancer patients because HPV interferes with local immunity suppressing the expression of inflammatory cytokines and chemokines in infected cells (28). Immunostimulatory cytokines like CCL2 and CCL20 are induced in the stromal compartment of invasive cervical carcinoma but they are involved in the generation of a pro-tumorigenic microenvironment (29)(30)(31). In contrast, the regulator of the adaptive immunity interleukin-12 is down-regulated in the cervical cancer microenvironment [own unpublished data and (32,33)].…”
Section: Discussionmentioning
confidence: 99%