The expression and clinical significance of microRNA-1258 and heparanase in human breast cancer

Tang, Dabei; Zhang, Qingyuan; Song, Zhao; Wang, Jincai; Lü, Kun; Song, Ying; Zhao, Ling; Kang, Xinmei; Wang, Jingxuan; Xu, Shanqi; Tian, Lantian

doi:10.1016/j.clinbiochem.2013.01.027

Cited by 55 publications

(31 citation statements)

References 37 publications

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“…Previous few studies identified that HPSE is a target of miR-1258 in breast [12, 13] and lung cancer [14]. However, there is no expression correlation between miR-1258 and HSPE in TCGA LIHC dataset, suggesting HSPE may not a critical target of miR-1258 in HCC (Figure S2).…”

Section: Discussionmentioning

confidence: 94%

“…However, the expression and critical role of miR-1258 in HCC have never been reported. Previous studies have showed that miR-1258 expression is attenuated in human breast cancer cells and patient tissues, and miR-1258 suppresses breast cancer brain metastasis by targeting heparanase (HSPE) [12, 13]. The miR-1258 has also been shown to inhibit the expression level of HPSE to influence the morbidity and metastasis of NSCLC.…”

Section: Discussionmentioning

confidence: 99%

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Loss of miR-1258 contributes to carcinogenesis and progression of liver cancer through targeting CDC28 protein kinase regulatory subunit 1B

Wang

et al. 2016

Oncotarget

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Hepatocellular carcinoma (HCC) is the leading cause of cancer related death worldwide. The number of deaths is proportional to the global incidence, which highlights the aggressive tumor biology and lack of effective therapies. Dysregulation of microRNAs has been implicated in carcinogenesis and progression of liver cancer. Here, we identified that miR-1258 was significantly downregulated in HCC and associated with poor patients' survival. Overexpression of miR-1258 significantly inhibits liver cancer cell growth, proliferation and tumorigenicity through increasing cell cycle arrest in G0/G1 phase and promotes cell apoptosis. Interestingly, stable overexpression of miR-1258 suppresses cell migration, stemness and increases sensitivity of HCC cells to chemotherapy drug like doxorubicin. The CDC28 protein kinase regulatory subunit 1B (CKS1B) was identified as a functional downstream target of miR-1258. Re-expression of CKS1B overcomes miR-1258 induced apoptosis and increases stemness of HCC cells, suggesting that loss of miR-1258 contributes to carcinogenesis and progression of liver cancer through targeting CKS1B. Therefore, loss of miR-1258 may be a potential diagnostic and prognostic biomarker and blocking miR-1258-CKS1B axis is a potential therapeutic strategy in HCC.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Loss of miR-1258 contributes to carcinogenesis and progression of liver cancer through targeting CDC28 protein kinase regulatory subunit 1B

Wang

et al. 2016

Oncotarget

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“…For example, elevated heparanase expression was associated with the lymph node status, late clinical stages, a short overall survival, and a short relapse-free survival with the highest heparanase levels in breast cancer those with lymph node metastasis. In addition, the serum heparanase levels of patients with metastatic breast cancer were significantly higher than primary breast cancer patients (119). By contrast, Fernandez-Vega and colleagues did not find any significant differences between heparanase expression in tumors and healthy tissue.…”

Section: Solid Tumorsmentioning

confidence: 99%

The Role of Heparanase and Sulfatases in the Modification of Heparan Sulfate Proteoglycans within the Tumor Microenvironment and Opportunities for Novel Cancer Therapeutics

Hammond¹,

et al. 2014

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Heparan sulfate proteoglycans (HSPGs) are an integral and dynamic part of normal tissue architecture at the cell surface and within the extracellular matrix. The modification of HSPGs in the tumor microenvironment is known to result not just in structural but also functional consequences, which significantly impact cancer progression. As substrates for the key enzymes sulfatases and heparanase, the modification of HSPGs is typically characterized by the degradation of heparan sulfate (HS) chains/sulfation patterns via the endo-6-O-sulfatases (Sulf1 and Sulf2) or by heparanase, an endo-glycosidase that cleaves the HS polymers releasing smaller fragments from HSPG complexes. Numerous studies have demonstrated how these enzymes actively influence cancer cell proliferation, signaling, invasion, and metastasis. The activity or expression of these enzymes has been reported to be modified in a variety of cancers. Such observations are consistent with the degradation of normal architecture and basement membranes, which are typically compromised in metastatic disease. Moreover, recent studies elucidating the requirements for these proteins in tumor initiation and progression exemplify their importance in the development and progression of cancer. Thus, as the influence of the tumor microenvironment in cancer progression becomes more apparent, the focus on targeting enzymes that degrade HSPGs highlights one approach to maintain normal tissue architecture, inhibit tumor progression, and block metastasis. This review discusses the role of these enzymes in the context of the tumor microenvironment and their promise as therapeutic targets for the treatment of cancer.

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“…Moreover, heparanase expression as determined by immunohistochemistry is associated with high-grade metastatic breast cancers [261] and with more invasive subtypes of human breast cancer as compared to less invasive subtypes [262]. Heparanase expression in breast cancer patients has also been associated with lymph node status, late clinical stages, a short overall survival and a short relapse-free survival [263]. …”

Section: Heparanase Syndecan-1 Shedding and Exosomes Facilitate Imentioning

confidence: 99%

Insights into the key roles of proteoglycans in breast cancer biology and translational medicine

Theocharis

Skandalis

Neill

et al. 2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

114

127

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Proteoglycans control numerous normal and pathological processes, among which are morphogenesis, tissue repair, inflammation, vascularization and cancer metastasis. During tumor development and growth, proteoglycan expression is markedly modified in the tumor microenvironment. Altered expression of proteoglycans on tumor and stromal cell membranes affects cancer cell signaling, growth and survival, cell adhesion, migration and angiogenesis. Despite the high complexity and heterogeneity of breast cancer, the rapid evolution in our knowledge that proteoglycans are among the key players in the breast tumor microenvironment suggests their potential as pharmacological targets in this type of cancer. It has been recently suggested that pharmacological treatment may target proteoglycan metabolism, their utilization as targets for immunotherapy or their direct use as therapeutic agents. The diversity inherent in the proteoglycans that will be presented herein provides the potential for multiple layers of regulation of breast tumor behavior. This review summarizes recent developments concerning the biology of selected proteoglycans in breast cancer, and presents potential targeted therapeutic approaches based on their novel key roles in breast cancer.

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The expression and clinical significance of microRNA-1258 and heparanase in human breast cancer

Cited by 55 publications

References 37 publications

Loss of miR-1258 contributes to carcinogenesis and progression of liver cancer through targeting CDC28 protein kinase regulatory subunit 1B

Loss of miR-1258 contributes to carcinogenesis and progression of liver cancer through targeting CDC28 protein kinase regulatory subunit 1B

The Role of Heparanase and Sulfatases in the Modification of Heparan Sulfate Proteoglycans within the Tumor Microenvironment and Opportunities for Novel Cancer Therapeutics

Insights into the key roles of proteoglycans in breast cancer biology and translational medicine

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