Heparanase-1-induced shedding of heparan sulfate from syndecan-1 in hepatocarcinoma cell facilitates lymphatic endothelial cell proliferation via VEGF-C/ERK pathway

Yu, Shengjin; Lv, Huiming; Zhang, He; Jiang, Yu; Hong, Yu; Xia, Rongjun; Zhang, Qifang; Ju, Weiwei; Jiang, Lili; Ou, Gang; Zhang, Jinhui; Wang, Shujing; Zhang, Jianing

doi:10.1016/j.bbrc.2017.02.060

Cited by 27 publications

(20 citation statements)

References 24 publications

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“…The repair response of tissue damage depends on intrinsic regenerative capacity and stem cells (12), the latter being reduced in patients with renal failure including HD patients (44). Increased markers of tissue repair have been reported in several renal studies such as VEGF (45), heparinbinding EGF (21), and syndecan-1 (2). Just like endothelial markers such as CD31 (26), increased plasma levels of syndecan-1 have been documented earlier in HD studies where it has been interpreted as an indicator for endothelial glycocalyx damage (43).…”

Section: Discussionmentioning

confidence: 99%

“…This is due to its crucial coreceptor function for regenerative growth factors such as vascular endothelial growth factor (VEGF) (45), insulin-like growth factor (IGF) (5), and its association with various integrins (37). By that, syndecan-1 is orchestrating proliferation (45), migration, and adhesion (37). Thus, depending on the stage and severity of the tissue damage, a positive association (initial disease) or a negative association (progressed disease) is found between injury and plasma (or tissue) syndecan-1 (2).…”

Section: Introductionmentioning

confidence: 99%

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Plasma syndecan-1 in hemodialysis patients associates with survival and lower markers of volume status

Koch

Idzerda

Dam

et al. 2019

American Journal of Physiology-Renal Physiology

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Syndecan-1, a transmembrane heparan sulfate proteoglycan, associates with renal and cardiovascular functioning. We earlier reported syndecan-1 to be involved in renal tubular regeneration. We now examined plasma values of syndecan-1 in a hemodialysis cohort and its association with volume and inflammatory and endothelial markers in addition to outcome. Eighty-four prevalent hemodialysis patients were evaluated for their plasma syndecan-1 levels by ELISA before the start of hemodialysis, as well as 60, 180, and 240 min after start of dialysis. Patients were divided into sex-stratified tertiles based on predialysis plasma syndecan-1 levels. We studied the association between plasma levels of syndecan-1 and volume, inflammation, and endothelial markers and its association with cardiovascular events and all-cause mortality using Kaplan-Meier curves and Cox regression analyses with adjustments for gender, age, diabetes, and dialysis vintage. Predialysis syndecan-1 levels were twofold higher in men compared with women ( P = 0.0003). Patients in the highest predialysis plasma syndecan-1 tertile had a significantly higher ultrafiltration rate ( P = 0.034) and lower plasma values of BNP ( P = 0.019), pro-ANP ( P = 0.024), and endothelin ( P < 0.0001) compared with the two lower predialysis syndecan-1 tertiles. No significant associations with inflammatory markers were found. Cox regression analysis showed that patients in the highest syndecan-1 tertile had significantly less cardiovascular events and better survival compared with the lowest syndecan-1 tertile ( P = 0.02 and P = 0.005, respectively). In hemodialysis patients, higher plasma syndecan-1 levels were associated with lower concentrations of BNP, pro-ANP, and endothelin and with better patient survival. This may suggest that control of volume status in hemodialysis patients allows an adaptive tissue regenerative response as reflected by higher plasma syndecan-1 levels.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma syndecan-1 in hemodialysis patients associates with survival and lower markers of volume status

Koch

Idzerda

Dam

et al. 2019

American Journal of Physiology-Renal Physiology

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“…The shedding of HS chains from SDC1 in hepatocarcinoma cells facilitates lymphatic endothelial cell proliferation through VEGF-C induced ERK signaling pathway [98]. In myeloma, SDC1-mediated activation of the VEGF receptor on adjacent endothelial cells promotes AKT and ERK signaling and stimulates tumor angiogenesis [192].…”

Section: Hspg-regulated Mechanisms In Cell-matrix and Cell-cell Intermentioning

confidence: 99%

“…However, TGF-β signaling may play a dual role in both pro-tumorigenic and tumor-suppressive of pancreatic cancer, depending on tumor stage and microenvironment [198]. Indeed, besides SMAD activation, TGF-β signaling can also be transduced The shedding of HS chains from SDC1 in hepatocarcinoma cells facilitates lymphatic endothelial cell proliferation through VEGF-C induced ERK signaling pathway [98]. In myeloma, SDC1-mediated activation of the VEGF receptor on adjacent endothelial cells promotes AKT and ERK signaling and stimulates tumor angiogenesis [192].…”

Section: Hspg-regulated Mechanisms In Cell-matrix and Cell-cell Intermentioning

confidence: 99%

Heparan Sulfate Proteoglycan Signaling in Tumor Microenvironment

Pasquale

Pavone

2020

IJMS

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In the last few decades, heparan sulfate (HS) proteoglycans (HSPGs) have been an intriguing subject of study for their complex structural characteristics, their finely regulated biosynthetic machinery, and the wide range of functions they perform in living organisms from development to adulthood. From these studies, key roles of HSPGs in tumor initiation and progression have emerged, so that they are currently being explored as potential biomarkers and therapeutic targets for cancers. The multifaceted nature of HSPG structure/activity translates in their capacity to act either as inhibitors or promoters of tumor growth and invasion depending on the tumor type. Deregulation of HSPGs resulting in malignancy may be due to either their abnormal expression levels or changes in their structure and functions as a result of the altered activity of their biosynthetic or remodeling enzymes. Indeed, in the tumor microenvironment, HSPGs undergo structural alterations, through the shedding of proteoglycan ectodomain from the cell surface or the fragmentation and/or desulfation of HS chains, affecting HSPG function with significant impact on the molecular interactions between cancer cells and their microenvironment, and tumor cell behavior. Here, we overview the structural and functional features of HSPGs and their signaling in the tumor environment which contributes to tumorigenesis and cancer progression.

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“…The significance of the expression of Sdc1 and its distribution and localization and association with established prognostic factors and prognostic value have been tested so far in pancreatic cancer [ 14 , 15 ], stomach cancer [ 16 – 18 ], colon cancer [ 19 , 20 ], liver cancer [ 21 ], prostate cancer [ 22 – 24 ], lung cancer [ 25 – 28 ], endometrial cancer [ 29 , 30 ], ovarian cancer [ 31 ], squamous head and neck cancer [ 32 – 36 ], melanoma [ 37 ], laryngeal cancer [ 38 ], cervical cancer [ 39 ], urothelial carcinoma of the bladder [ 40 ], multiple myeloma [ 5 , 41 – 43 ], and breast cancer [ 44 – 46 ] where its overexpression generally means a poor prognosis, although various studies have shown conflicting results.…”

Section: Introductionmentioning

confidence: 99%

Comparison of Syndecan-1 Immunohistochemical Expression in Lobular and Ductal Breast Carcinoma with Nodal Metastases

Miše

Vučić

2018

Analytical Cellular Pathology

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Syndecan-1 (Sdc1) is a transmembrane heparan sulfate proteoglycan, an extracellular matrix receptor involved in intercellular communication, proliferation, angiogenesis, and metastasis. This study determined and compared Sdc1 expression in the tumor cells and stroma of 30 invasive lobular and 30 invasive ductal breast carcinomas (ILCs/IDCs), also in the axillary node metastases of ductal type, and correlated it with clinical and tumor parameters. Sdc1 was expressed in the epithelium of 90% carcinoma of both histological types. Also, it was most frequently expressed in their tumor stroma, but in ILC, stromal expression was negative in 40%. Sdc1 was expressed in 86.7% of the metastatic epithelium of IDC nodal metastases (in even 50% as high expression), while the nodal stroma was negative in 46.7%. Primary IDC showed a negative correlation between epithelial Sdc1 and progesterone receptors (PRs), whereas ILC showed a positive correlation between stromal Sdc1 and histological gradus. In the metastatic epithelium, Sdc1 was negatively correlated with a patient's age, estrogen receptors (ERs), and PRs in the primary tumors, while the stroma of metastases demonstrated a positive correlation with the focus number in primary tumors and a negative correlation with PRs in primary tumors. This research revealed identical overall epithelial Sdc1 expression in both breast carcinomas with no statistically significant difference in its stromal expression and confirmed the role of Sdc1 in the progression of both tumor types and in the development of ductal carcinoma's metastatic potential.

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Heparanase-1-induced shedding of heparan sulfate from syndecan-1 in hepatocarcinoma cell facilitates lymphatic endothelial cell proliferation via VEGF-C/ERK pathway

Cited by 27 publications

References 24 publications

Plasma syndecan-1 in hemodialysis patients associates with survival and lower markers of volume status

Plasma syndecan-1 in hemodialysis patients associates with survival and lower markers of volume status

Heparan Sulfate Proteoglycan Signaling in Tumor Microenvironment

Comparison of Syndecan-1 Immunohistochemical Expression in Lobular and Ductal Breast Carcinoma with Nodal Metastases

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