MDA-9/Syntenin/SDCBP: new insights into a unique multifunctional scaffold protein

Pradhan, Anjan K.; Maji, Santanu; Das, Swadesh K.; Emdad, Luni; Sarkar, Devanand; Fisher, Paul B.

doi:10.1007/s10555-020-09886-7

Cited by 30 publications

(28 citation statements)

References 97 publications

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“…Additionally, syntenin-1 (syndecan binding protein, SDCBP or MDA9), which is important for syndecan signaling, has also been involved in cancer progression. SDCBP shows increasing expression in tumor progression from localized to metastatic lesions [30,31]. As mentioned above, SDCBP binds to the conserved syndecan C2 via its PDZ domains [31].…”

Section: Introductionmentioning

confidence: 91%

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Syndecan Family Gene and Protein Expression and Their Prognostic Values for Prostate Cancer

Santos

Barquilha

Barbosa

et al. 2021

IJMS

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Prostate cancer (PCa) is the leading cause of cancer-associated mortality in men, and new biomarkers are still needed. The expression pattern and protein tissue localization of proteoglycans of the syndecan family (SDC 1–4) and syntenin-1 (SDCBP) were determined in normal and prostatic tumor tissue from two genetically engineered mouse models and human prostate tumors. Studies were validated using SDC 1–4 and SDCBP mRNA levels and patient survival data from The Cancer Genome Atlas and CamCAP databases. RNAseq showed increased expression of Sdc1 in Pb-Cre4/Ptenf/f mouse Pca and upregulation of Sdc3 expression and downregulation of Sdc2 and Sdc4 when compared to the normal prostatic tissue in Pb-Cre4/Trp53f/f-;Rb1f/f mouse tumors. These changes were confirmed by immunohistochemistry. In human PCa, SDC 1–4 and SDCBP immunostaining showed variable localization. Furthermore, Kaplan–Meier analysis showed that patients expressing SDC3 had shorter prostate-specific survival than those without SDC3 expression (log-rank test, p = 0.0047). Analysis of the MSKCC-derived expression showed that SDC1 and SDC3 overexpression is predictive of decreased biochemical recurrence-free survival (p = 0.0099 and p = 0.045, respectively), and SDC4 overexpression is predictive of increased biochemical recurrence-free survival (p = 0.035). SDC4 overexpression was associated with a better prognosis, while SDC1 and SDC3 were associated with more aggressive tumors and a worse prognosis.

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Section: Introductionmentioning

confidence: 91%

“…SDCBP shows increasing expression in tumor progression from localized to metastatic lesions [30,31]. As mentioned above, SDCBP binds to the conserved syndecan C2 via its PDZ domains [31]. There is no information on the affinity of SDCBP to the different syndecans.…”

Section: Introductionmentioning

confidence: 99%

Syndecan Family Gene and Protein Expression and Their Prognostic Values for Prostate Cancer

Santos

Barquilha

Barbosa

et al. 2021

IJMS

View full text Add to dashboard Cite

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“…Syntenin-1 is a PDZ domain-containing molecule, which was identified as a key oncogene in melanoma. Moreover, different types of cancer, including glioblastoma; neuroblastoma; and prostate, breast, and liver cancer exhibit aberrant expression of syntenin-1 [ 142 ]. Recent findings demonstrated that, through phosphorylation of STAT3, syntenin-1 increases the expression of PD-L1 in both breast cancer cell lines and in tumor tissues derived from patients with TNBC cocultured with T CD8+ cells.…”

Section: Epithelial-mesenchymal Transition Factors That Determine mentioning

confidence: 99%

Determining Factors in the Therapeutic Success of Checkpoint Immunotherapies against PD-L1 in Breast Cancer: A Focus on Epithelial-Mesenchymal Transition Activation

Segovia-Mendoza

Romero-García

Lemini

et al. 2021

Journal of Immunology Research

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Breast cancer is the most common neoplasm diagnosed in women around the world. Checkpoint inhibitors, targeting the programmed death receptor-1 or ligand-1 (PD-1/PD-L1) axis, have dramatically changed the outcome of cancer treatment. These therapies have been recently considered as alternatives for treatment of breast cancers, in particular those with the triple-negative phenotype (TNBC). A further understanding of the regulatory mechanisms of PD-L1 expression is required to increase the benefit of PD-L1/PD-1 checkpoint immunotherapy in breast cancer patients. In this review, we will compile the most recent studies evaluating PD-1/PD-L1 checkpoint inhibitors in breast cancer. We review factors that determine the therapeutic success of PD-1/PD-L1 immunotherapies in this pathology. In particular, we focus on pathways that interconnect the epithelial-mesenchymal transition (EMT) with regulation of PD-L1 expression. We also discuss the relationship between cellular metabolic pathways and PD-L1 expression that are involved in the promotion of resistance in TNBC.

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“…The melanoma-differentiation associated protein 9 (MDA-9, also called Syntenin-1) is another ECM protein that sponsors tumor invasion mainly by regulating the cell surface receptor Syndecan ( 113 ). In GBM, MDA-9 expression is an important regulator of cell invasion ( 114 ), stemness phenotype, and survival of GSCs through STAT3 and Notch1 pathways, respectively ( 115 ).…”

Section: Autophagy Activation As a Response To Physiological Signalsmentioning

confidence: 99%

A Key Pathway to Cancer Resilience: The Role of Autophagy in Glioblastomas

et al. 2021

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There are no effective strategies for the successful treatment of glioblastomas (GBM). Current therapeutic modalities effectively target bulk tumor cells but leave behind marginal GBM cells that escape from the surgical margins and radiotherapy field, exhibiting high migratory phenotype and resistance to all available anti-glioma therapies. Drug resistance is mostly driven by tumor cell plasticity: a concept associated with reactivating transcriptional programs in response to adverse and dynamic conditions from the tumor microenvironment. Autophagy, or “self-eating”, pathway is an emerging target for cancer therapy and has been regarded as one of the key drivers of cell plasticity in response to energy demanding stress conditions. Many studies shed light on the importance of autophagy as an adaptive mechanism, protecting GBM cells from unfavorable conditions, while others recognize that autophagy can kill those cells by triggering a non-apoptotic cell death program, called ‘autophagy cell death’ (ACD). In this review, we carefully analyzed literature data and conclude that there is no clear evidence indicating the presence of ACD under pathophysiological settings in GBM disease. It seems to be exclusively induced by excessive (supra-physiological) stress signals, mostly from in vitro cell culture studies. Instead, pre-clinical and clinical data indicate that autophagy is an emblematic example of the ‘dark-side’ of a rescue pathway that contributes profoundly to a pro-tumoral adaptive response. From a standpoint of treating the real human disease, only combinatorial therapy targeting autophagy with cytotoxic drugs in the adjuvant setting for GBM patients, associated with the development of less toxic and more specific autophagy inhibitors, may inhibit adaptive response and enhance the sensibility of glioma cells to conventional therapies.

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MDA-9/Syntenin/SDCBP: new insights into a unique multifunctional scaffold protein

Cited by 30 publications

References 97 publications

Syndecan Family Gene and Protein Expression and Their Prognostic Values for Prostate Cancer

Syndecan Family Gene and Protein Expression and Their Prognostic Values for Prostate Cancer

Determining Factors in the Therapeutic Success of Checkpoint Immunotherapies against PD-L1 in Breast Cancer: A Focus on Epithelial-Mesenchymal Transition Activation

A Key Pathway to Cancer Resilience: The Role of Autophagy in Glioblastomas

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