CD147 Is a Promising Target of Tumor Progression and a Prognostic Biomarker

Landras, Alexandra; Moura, Coralie Reger de; Jouenne, Fanélie; Lebbe, Célèste; Ménashi, Suzanne; Mourah, Samia

doi:10.3390/cancers11111803

Cited by 106 publications

(103 citation statements)

References 124 publications

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“…However, effective immunotherapies, whether they are adoptive cell therapy or checkpoint blockade‐based approaches, have been limited for patients because of immunosuppressive barriers that exist in TME. The TME is known to be essential to the onset, development, progression, and relapse of many types of cancers 27 . Thus, deeper explorations of the complexities within the TME may help to reveal novel biomarkers that could facilitate increased accuracy of prognosis for patients and their potential responsiveness to immunotherapy as well as improve therapeutic modulation.…”

Section: Discussionmentioning

confidence: 99%

Development of an IFNγ response‐related signature for predicting the survival of cutaneous melanoma

Qian

et al. 2020

Cancer Medicine

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Background The tumor microenvironment (TME) plays a critical role in tumorigenesis, development, and therapeutic efficacy. Major advances have been achieved in the treatment of various cancers through immunotherapy. Nevertheless, only a minority of patients have positive responses to immunotherapy, which is partly due to conditions of the immunosuppressive microenvironment. Therefore, it is essential to identify prognostic biomarkers that reflect heterogeneous landscapes of the TME. Methods and materials Based upon the ESTIMATE algorithm, we evaluated the infiltrating levels of immune and stromal components derived from patients afflicted by various types of cancer from The Cancer Genome Atlas database (TCGA). According to respective patient immune and stromal scores, we categorized cases into high‐ and low‐scoring subgroups for each cancer type to explore associations between TME and patient prognosis. Gene Set Enrichment Analyses (GSEA) were conducted and genes enriched in IFNγ response signaling pathway were selected to facilitate establishment of a risk model for predicting overall survival (OS). Furthermore, we investigated the associations between the prognostic signature and tumor immune infiltration landscape by using CIBERSORT algorithm and TIMER database. Results Among the cancers assessed, the immune scores for skin cutaneous melanoma (SKCM) were the most significantly correlated with patients' survival time (P < .0001). We identified and validated a five‐IFNγ response‐related gene signature (UBE2L6, PARP14, IFIH1, IRF2, and GBP4), which was closely correlated with the prognosis for SKCM afflicted patients. Multivariate Cox regression analysis indicated that this risk model was an independent prognostic factor for SKCM. Tumor‐infiltrating lymphocytes and specific immune checkpoint molecules had notably differential levels of expression in high‐ compared to low‐risk samples. Conclusion In this study, we established a novel five‐IFNγ response‐related gene signature that provided a better and increasingly comprehensive understanding of tumor immune landscape, and which demonstrated good performance in predicting outcomes for patients afflicted by SKCM.

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Section: Discussionmentioning

confidence: 99%

Development of an IFNγ response‐related signature for predicting the survival of cutaneous melanoma

Qian

et al. 2020

Cancer Medicine

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“…The potential involvement of tumor-derived sEVs in the process of CR-CSC differentiation is also poorly understood and may be a key point to explore given that the differentiation of CR-CSC could be an attractive therapeutic strategy. Dai et al demonstrated that subpopulations of tumor cell lines that constitutively express high levels of cell-surface CD147 exhibit cancer stem-like cell features and Yoshioka and colleagues confirmed a high level of CD147 expression in EVs isolated from CRC cell lines [13,33]. Despite the interest in CD147, its involvement in the differentiation of CR-CSC and in the effects of sEV on recipient cells has not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…CD147 is a glycoprotein released by tumor cells and transferred to surrounding cells (both cancer cells and TME) in soluble form or by EVs [12]. CD147-sEVs have been identified in ovarian and bladder cancer, and recent evidence suggests that circulating CD147-containing EVs might be used as a biomarker to monitor response to therapy in CRC patients, but no study so far has analyzed the CD147 fate during colorectal cancer stem cell lines (CR-CSCs) differentiation [13][14][15][16]. This study aimed to analyze the role of sEVs in the differentiation process of CR-CSC and to understand whether CD147-sEVs could be involved in differentiation therapy inefficacy.…”

Section: Introductionmentioning

confidence: 99%

CD147 Promotes Cell Small Extracellular Vesicles Release during Colon Cancer Stem Cells Differentiation and Triggers Cellular Changes in Recipient Cells

Lucchetti

Colella

Perelli

et al. 2020

Cancers

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Cancer cells secrete small extracellular vesicles (sEVs) that are involved in the remodeling of tumor microenvironment (TME) and can promote tumor progression. The role of sEVs and their molecular key players in colon cancer stem cells differentiation are poorly understood. This study aimed to analyze the role and content of sEVs released during the differentiation of colorectal cancer stem cells. Here we show that sEVs secretion during colon cancer stem cells differentiation is partially controlled by CD147, a well-known player involved in colon cancer tumorigenesis. CD147 + sEVs activate a signaling cascade in recipient cells inducing molecular invasive features in colon cancer cells. CD147 knockdown as well as anti-CD147 antibodies impaired sEVs release and downstream effects on recipient cells and blocking multivesicular body maturation prevented sEVs release during the differentiation. Our findings reveal a functional role of CD147 in promoting sEVs release during the differentiation of colon cancer stem cells and in triggering cellular changes in recipient cells.

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“…Most importantly, we found that CD147 could facilitate collective invasion. Previous studies have shown that CD147 promotes tumor cell adhesion, migration and invasion in various kinds of cancers [40] and the underlying mechanisms are diverse depending on the type of cancer and are not fully understood. We and others have found that enriched expression of CD147 on the surface of tumor cells induces stromal and tumor cells themselves to increase MMPs expression and secretion, leading to the degradation of the surrounding stroma [30,41].…”

Section: Discussionmentioning

confidence: 99%

CD147 promotes collective invasion through cathepsin B in hepatocellular carcinoma

Wang

Chen

Wei

et al. 2020

Preprint

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Background Mounting evidence suggests that solid tumors display the features of collective invasion, however, the molecular mechanisms are far from clear. This study aims to verify the role and the underlying mechanisms of CD147 in collective invasion in hepatocellular carcinoma. Methods Immunostaining was used to analyze human hepatocellular carcinoma specimens and three-dimensional cultures. Three-dimensional invasion model was established to mimic in vivo invasion. RNA-sequencing was used to identify downstream effectors. Results Human hepatocellular carcinoma undergone collective invasion and CD147 was observed to be upregulated at the invasive front of tumor cell groups. CD147 was demonstrated to promote collective invasion using the modified three-dimensional invasion model, which recapitulated the main features of collective invasion. Through transcriptome analysis and enzyme activity assay, we found that CD147 enhanced cathepsin B expression and activation. Upregulated cathepsin B in hepatocellular carcinoma cells facilitated migration and invasion, which mediated CD147-induced invasive phenotype in hepatocellular carcinoma. In terms of mechanism, we found that CD147 promoted cathepsin B transcription by activating β-catenin signaling as a result of reduced GSK-3β expression. Furthermore, we found that elevated expression of CD147 as well as cathepsin B were correlated with poor prognosis in patients with hepatocellular carcinoma. Conclusions CD147 promotes hepatocellular carcinoma cells collective invasion via upregulating cathepsin B expression and targeting CD147 would be valuable for the development of novel therapeutic modalities against invasion and metastasis of cancer.

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CD147 Is a Promising Target of Tumor Progression and a Prognostic Biomarker

Cited by 106 publications

References 124 publications

Development of an IFNγ response‐related signature for predicting the survival of cutaneous melanoma

Development of an IFNγ response‐related signature for predicting the survival of cutaneous melanoma

CD147 Promotes Cell Small Extracellular Vesicles Release during Colon Cancer Stem Cells Differentiation and Triggers Cellular Changes in Recipient Cells

CD147 promotes collective invasion through cathepsin B in hepatocellular carcinoma

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