Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities
Cell surface glycosylation is dynamic and often changes in response to cellular differentiation under physiological or pathophysiological conditions. Altered glycosylation on cancers cells is gaining attention due its wide-spread occurrence across a variety of cancer types and recent studies that ha...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2018-06-01
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| Series: | Cancers |
| Subjects: | |
| Online Access: | http://www.mdpi.com/2072-6694/10/6/207 |
| _version_ | 1797706476956942336 |
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| author | Emily Rodrigues Matthew S. Macauley |
| author_facet | Emily Rodrigues Matthew S. Macauley |
| author_sort | Emily Rodrigues |
| collection | DOAJ |
| description | Cell surface glycosylation is dynamic and often changes in response to cellular differentiation under physiological or pathophysiological conditions. Altered glycosylation on cancers cells is gaining attention due its wide-spread occurrence across a variety of cancer types and recent studies that have documented functional roles for aberrant glycosylation in driving cancer progression at various stages. One change in glycosylation that can correlate with cancer stage and disease prognosis is hypersialylation. Increased levels of sialic acid are pervasive in cancer and a growing body of evidence demonstrates how hypersialylation is advantageous to cancer cells, particularly from the perspective of modulating immune cell responses. Sialic acid-binding receptors, such as Siglecs and Selectins, are well-positioned to be exploited by cancer hypersialylation. Evidence is also mounting that Siglecs modulate key immune cell types in the tumor microenvironment, particularly those responsible for maintaining the appropriate inflammatory environment. From these studies have come new and innovative ways to block the effects of hypersialylation by directly reducing sialic acid on cancer cells or blocking interactions between sialic acid and Siglecs or Selectins. Here we review recent works examining how cancer cells become hypersialylated, how hypersialylation benefits cancer cells and tumors, and proposed therapies to abrogate hypersialylation of cancer. |
| first_indexed | 2024-03-12T05:51:49Z |
| format | Article |
| id | doaj.art-b9aa3595e2d448938507ec05ec306180 |
| institution | Directory Open Access Journal |
| issn | 2072-6694 |
| language | English |
| last_indexed | 2024-03-12T05:51:49Z |
| publishDate | 2018-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cancers |
| spelling | doaj.art-b9aa3595e2d448938507ec05ec3061802023-09-03T05:02:43ZengMDPI AGCancers2072-66942018-06-0110620710.3390/cancers10060207cancers10060207Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic OpportunitiesEmily Rodrigues0Matthew S. Macauley1Department of Chemistry, University of Alberta, Edmonton, AB T6G 2G2, CanadaDepartment of Chemistry, University of Alberta, Edmonton, AB T6G 2G2, CanadaCell surface glycosylation is dynamic and often changes in response to cellular differentiation under physiological or pathophysiological conditions. Altered glycosylation on cancers cells is gaining attention due its wide-spread occurrence across a variety of cancer types and recent studies that have documented functional roles for aberrant glycosylation in driving cancer progression at various stages. One change in glycosylation that can correlate with cancer stage and disease prognosis is hypersialylation. Increased levels of sialic acid are pervasive in cancer and a growing body of evidence demonstrates how hypersialylation is advantageous to cancer cells, particularly from the perspective of modulating immune cell responses. Sialic acid-binding receptors, such as Siglecs and Selectins, are well-positioned to be exploited by cancer hypersialylation. Evidence is also mounting that Siglecs modulate key immune cell types in the tumor microenvironment, particularly those responsible for maintaining the appropriate inflammatory environment. From these studies have come new and innovative ways to block the effects of hypersialylation by directly reducing sialic acid on cancer cells or blocking interactions between sialic acid and Siglecs or Selectins. Here we review recent works examining how cancer cells become hypersialylated, how hypersialylation benefits cancer cells and tumors, and proposed therapies to abrogate hypersialylation of cancer.http://www.mdpi.com/2072-6694/10/6/207sialic acidSiglecSelectininflammationlectinglycosylationtumor-associated macrophageimmunosurveillance |
| spellingShingle | Emily Rodrigues Matthew S. Macauley Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities Cancers sialic acid Siglec Selectin inflammation lectin glycosylation tumor-associated macrophage immunosurveillance |
| title | Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities |
| title_full | Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities |
| title_fullStr | Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities |
| title_full_unstemmed | Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities |
| title_short | Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities |
| title_sort | hypersialylation in cancer modulation of inflammation and therapeutic opportunities |
| topic | sialic acid Siglec Selectin inflammation lectin glycosylation tumor-associated macrophage immunosurveillance |
| url | http://www.mdpi.com/2072-6694/10/6/207 |
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