CCL18 from tumor‐cells promotes epithelial ovarian cancer metastasis via mTOR signaling pathway

Wang, Qi; Tang, Yong; Yu, Hongjing; Yin, Qiaoyun; Li, Mengdi; Shi, Lijun; Zhang, Wei; Li, Danrong; Li, Li

doi:10.1002/mc.22419

Cited by 59 publications

(42 citation statements)

References 46 publications

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“…The knockdown of CXCR4 in CC cells leads to a decrease in cell migration [34]. CCL18 enhances proliferation and metastasis of ovarian cancer cell lines [35]. Furthermore, downregulation of VEGFC expression in CC cells decelerates tumor growth and inhibits metastasis [36].…”

Section: Discussionmentioning

confidence: 99%

High expression of WISP1 in colon cancer is associated with apoptosis, invasion and poor prognosis

Long

Cai

et al. 2016

Oncotarget

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Colon cancer (CC) likes many epithelial-derived cancers, resulting from a complex tumorigenic process. However, the exactly mechanisms of development and progression of CC are still unknown. In this study, integrated analysis in the GSE33113 and Fudan University Shanghai Cancer Center Hospital datasets revealed that WISP1 expression was significantly increased in CC cases, positivity correlated with the advanced pathologic stage and a poor prognosis was more likely in CC patients with higher levels of WISP1. Downregulation of WISP1 inhibited cell proliferation and invasion through increasing apoptosis and blocking cell cycle at G1 phase in CC LOVO and RKO cells. Besides, Gene set enrichment analysis (GSEA) revealed that relative genes involved in the Cell adhesion molecules and Cytokine-cytokine receptor interaction pathways were enriched in WISP1-higher expression patients. Western blot analysis showed that Cell adhesion molecules pathway associated genes (ICAM- 1, VCAM-1, SDC2 and CDH2) and Cytokine-cytokine receptor interaction pathway associated genes (VEGFC, CCL18, CXCR4 and TGFBR1) were also modulated by WISP1 downregulation. Then, we found that the protein β-catenin was identified as a binding partner of WISP1 and mediated the functions of WISP1 through promoting cell proliferation and invasion in LOVO and RKO cells. Further in vivo tumor formation study in nude mice indicated that inhibition of WISP1 delayed the progress of tumor formation and inhibited PCNA expression. These results indicate that WISP1 could act as an oncogene and may serve as a promising therapeutic strategy for colon cancer.

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Section: Discussionmentioning

confidence: 99%

High expression of WISP1 in colon cancer is associated with apoptosis, invasion and poor prognosis

Long

Cai

et al. 2016

Oncotarget

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“…Finally in the ovarian cancer cell line Skov3, CCL18 ectopic expression endows tumor cells with enhanced migratory and invasive properties in vitro (although the authors do not investigate the expression of any marker or transcription factor linked to EMT) (Wang et al ., ).…”

Section: Emt and Soluble Factors Of Inflammationmentioning

confidence: 97%

“…CCL5 and CCR5 expressions are also associated with ovarian cancer metastasis (Long et al ., ). CCL18, which induces EMT in ovarian cancer cells in vitro , is also associated with high tumor grade and metastasis in patients with ovarian cancer (Wang et al ., ). High EMT/hypoxia‐associated CCL20 expression has been associated with poor patient DFS and OS in a cohort of 90 hepatocellular carcinomas (Ye et al ., ).…”

Section: Emt Inflammation and The Metastatic Progressionmentioning

confidence: 97%

EMT and inflammation: inseparable actors of cancer progression

et al. 2017

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Tumors can be depicted as wounds that never heal, and are infiltrated by a large array of inflammatory and immune cells. Tumor‐associated chronic inflammation is a hallmark of cancer that fosters progression to a metastatic stage, as has been extensively reviewed lately. Indeed, inflammatory cells persisting in the tumor establish a cross‐talk with tumor cells that may result in a phenotype switch into tumor‐supporting cells. This has been particularly well described for macrophages and is referred to as tumor‐associated ‘M2’ polarization. Epithelial‐to‐mesenchymal transition (EMT), the embryonic program that loosens cell–cell adherence complexes and endows cells with enhanced migratory and invasive properties, can be co‐opted by cancer cells during metastatic progression. Cancer cells that have undergone EMT are more aggressive, displaying increased invasiveness, stem‐like features, and resistance to apoptosis. EMT programs can also stimulate the production of proinflammatory factors by cancer cells. Conversely, inflammation is a potent inducer of EMT in tumors. Therefore, the two phenomena may sustain each other, in an alliance for metastasis. This is the focus of this review, where the interconnections between EMT programs and cellular and molecular actors of inflammation are described. We also recapitulate data linking the EMT/inflammation axis to metastasis.

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“…CCL18 inhibits cutaneous T cell proliferation 111 . In some cancers, such as breast cancer, the main source of CCL18 in the tumour is TAMs, whereas ovarian cancer cells can overexpress CCL18 (REFS 105,106). Although not shown in cancer, CCL18 has an immunosuppressive effect on DCs and macrophages 112–115 .…”

Section: Effects Of Chemokines On Tumour Cellsmentioning

confidence: 99%

Chemokines in the cancer microenvironment and their relevance in cancer immunotherapy

2017

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The tumour microenvironment is the primary location in which tumour cells and the host immune system interact. Different immune cell subsets are recruited into the tumour microenvironment via interactions between chemokines and chemokine receptors, and these populations have distinct effects on tumour progression and therapeutic outcomes. In this Review, we focus on the main chemokines that are found in the human tumour microenvironment; we elaborate on their patterns of expression, their regulation and their roles in immune cell recruitment and in cancer and stromal cell biology, and we consider how they affect cancer immunity and tumorigenesis. We also discuss the potential of targeting chemokine networks, in combination with other immunotherapies, for the treatment of cancer.

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CCL18 from tumor‐cells promotes epithelial ovarian cancer metastasis via mTOR signaling pathway

Cited by 59 publications

References 46 publications

High expression of WISP1 in colon cancer is associated with apoptosis, invasion and poor prognosis

High expression of WISP1 in colon cancer is associated with apoptosis, invasion and poor prognosis

EMT and inflammation: inseparable actors of cancer progression

Chemokines in the cancer microenvironment and their relevance in cancer immunotherapy

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