The use of heparin and heparin-like molecules in cancer treatment: a review

Atallah, Johnny; Khachfe, Hussein H.; Berro, Juliett; Assi, Hazem

doi:10.1016/j.ctarc.2020.100192

Cited by 40 publications

(33 citation statements)

References 54 publications

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“…The results identi ed many pathways related to cancer. Including PI3K-Akt signaling pathway [27],Human papillomavirus infection [28],ECM-receptor interaction [29],Proteoglycans in cancer [30],MAPK signaling pathway [31],TGF-beta signaling pathway [32],cGMP-PKG signaling pathway [33],Small cell lung cancer,transmembrane receptor protein serine/threonine [34],kinase signaling pathway [35],focal adhesion [36],endoplasmic reticulum lumen [37],basement membrane [38],extracellular matrix [39],integrinbinding [40],heparin-binding [41],growth factor binding [42] and glycosaminoglycan binding [43].A large number of studies have con rmed that it is related to the occurrence and development of tumors and tumor immune in ltration.…”

Section: Discussionmentioning

confidence: 99%

CHSY3 As A Potential Therapeutic Target For Gastric Cancer

Fan

Huang

Liang

et al. 2022

Preprint

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Background: Chondroitin synthase 3(CHSY3) has been reported to be closely related to the occurrence, development, recurrence, and metastasis of a variety of cancers. But its role in gastric cancer (GC) has not been studied. Methods: Tumor Immune Estimate Resource (TIMER), The Cancer Genome Atlas (TCGA), and Gene Expression Omnibus (GEO) were used to detect the expression of CHSY3 in gastric cancer. Analyze the correlation between CHSY3 expression and clinicopathological parameters. Draw a Kaplan-Meier survival curve to detect the clinical prognostic significance of CHSY3 in gastric cancer. Meta-analysis of the above results to determine the role of CHSY3 in GC.COX regression analysis was used to study whether CHSY3 is a predictor of GC patients. Analyze the methylation data from the TCGA database to determine the sites with a significant correlation. Through GO analysis and KEGG analysis to study the regulation mechanism of CHSY3 related genes. Screen 3 genes (APOD, GJA1, SERPINE1) from the related genes of CHSY3 as a predictive signature.Constructed a nomogram to predict the 1-year and 3-year survival probability of GC patients. The TIMER database was used to study the correlation between CHSY3 and tumor infiltrating immune cells.Study the drug sensitivity of CHSY3 related genes by using Gene Set Cancer Analysis (GSCA).Results: CHSY3 was highly expressed in GC and significantly correlated with the T stage.The higher the expression level of CHSY3 in GC, the higher the methylation level of cg06610705 and cg11572844,which suggests that patients with gastric cancer have a poorer prognosis.Enrichment analysis identified multiple cancer-related pathways, for example, PI3K-Akt signaling pathway,MAPK signaling pathway, and TGF-beta signaling pathway.The risk score has a very high predictive value.CHSY3 is closely associated with CD4+ T cells, macrophages, neutrophils, and dendritic.Besides,different mutational forms of CHSY3 were associated with the immune infiltration of 6 leukocytes.In addition,CHSY3 may contribute to drug resistance in GC.Conclusion: CHSY3 may be a potential prognostic biomarker for gastric cancer, and it can be used as a new therapeutic target for the treatment of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

CHSY3 As A Potential Therapeutic Target For Gastric Cancer

Fan

Huang

Liang

et al. 2022

Preprint

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“…Interaction between molecules expressed by cancer cells and factors in the tumor microenvironment can affect proliferation and survival, adhesion, migration of tumor cells, and tumor invasion and metastasis (38). Heparin is a part of glycosaminoglycan, and derivatives of this molecule can signi cantly reduce BC cell proliferation and metastasis both in vitro and in vivo (39). Receptors, especially hormone receptors, are important in the biology of BC, and ER/PR are involved in the development and progression of BC.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of lncRNA LINC00968 may contribute to the tumorigenesis of estrogen receptor-positive (ER+) breast cancer

Arabpour

Layeghi

Majidzadeh‐A

et al. 2022

Preprint

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Background: Estrogen receptor-positive (ER+) breast cancer (BC) (luminal A and B subtypes) comprises up to 70% of all BC patients. LncRNAs can affect many biological and pathological processes, and dysregulation of them is related to human cancers. The potential role of lncRNA LINC00968 in ER+ BC is still unclear. Methods: We analyzed the LINC00968 expression across 44 paired luminal BC tissues from the TCGA-BRCA RNA sequencing dataset, and we used the GEPIA2 web server and GENEVESTIGATOR software, as well. The qRT-PCR assay was performed to confirm the LINC00968 expression in 71 paired luminal BC tissues and two luminal A cell lines (MCF7 and T47D). Moreover, to better understand the potential function of LINC00968 in luminal BC, multiple in silico data analyses have been done including co-expression, functional enrichment, and genetic alteration analyses. Results: The results of data analyses retrieved from BRCA dataset and databases revealed the significant downregulation of LINC00968 in luminal A and B BC. Also, the results of qRT-PCR in luminal BC tissues and cell lines confirmed the earlier data. LINC00968 expression was negatively associated with tumor stage and lymph node metastasis. Additionally, functional annotation analyses revealed that LINC00968 might be involved in vascular development and angiogenesis, extracellular matrix organization, and cell motility and migration. LINC00968 might have functions in some cancer-related signaling pathways, like the PPAR signaling pathway, small ligand GPCRs, etc. Conclusions: Our study found that LINC00968 may be a potential tumor suppressor gene in luminal BC. Downregulation of LINC00968 might promote tumorigenesis, invasion, and metastasis of luminal BC.

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“…Chemoresistant tumors are characterized by increased expression of collagens and collagen-stabilizing enzymes such as lysyl oxidase (LOX). Similarly, the high-water content of hyaluronic-rich pancreas tumors, sarcomas or glioblastoma creates a high interstitial pressure, interfering with drug distribution (34). Finally, the therapy with therapeutic antibodies is strongly restricted by the rigid ECM.…”

Section: Discussionmentioning

confidence: 99%

Fibrin and Extracellular Matrix: Scaffolds and Network for Malignant Cells

Schardt

Schmausser

Bedel

et al. 2021

MRAJ

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Malignant cells build up a protective shield in form of a fibrin meshwork surrounding the tumor which helps it to escape the body’s immune system. In addition, tumor and stromal cells provide with an abundant extracellular matrix (ECM) consisting of proteoglycans, collagens, glycoproteins and glucosaminoglycans an additional scaffold with the capacity to bind large quantities of immunsuppressive substances. Many investigations found that heparin has a wide variety of positive effects counteracting these shielding and immunosuppressive properties of the ECM. Heparin can bind and neutralize many protective substances produced by the tumor cells. It inhibits cross-linking of collagen by deamination, and reduces the expression of FAK, LOX, glucosamines and proteoglycans. By these actions it prevents the development of a stiff and rigid ECM which presents additionally an effective scaffold for the tumor cells and also reduce the efficiency of therapeutic methods. In an ambulant trial with exogenously-added heparin in high dosages the survival probability over three years was significantly higher than without (p<0.001). Therefore, a combined therapy with a fibrinolyticum and heparin should be considered. This auxiliary treatment has the potential to support established therapy and improve anti-tumor response by the immune system.

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The use of heparin and heparin-like molecules in cancer treatment: a review

Cited by 40 publications

References 54 publications

CHSY3 As A Potential Therapeutic Target For Gastric Cancer

CHSY3 As A Potential Therapeutic Target For Gastric Cancer

Dysregulation of lncRNA LINC00968 may contribute to the tumorigenesis of estrogen receptor-positive (ER+) breast cancer

Fibrin and Extracellular Matrix: Scaffolds and Network for Malignant Cells

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