Breast cancer metastasis: Putative therapeutic role of vascular cell adhesion molecule-1

Sharma, Rohit; Sharma, Rohini; Khaket, Tejinder Pal; Dutta, Chanchala; Chakraborty, Bornisha; Mukherjee, Tapan Kumar

doi:10.1007/s13402-017-0324-x

Cited by 112 publications

(70 citation statements)

References 73 publications

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“…Uncoupling of M-E reversion from FN expression explains why FN high tumor cells can repeatedly be isolated from macrometastatic foci in distant organs [77]. Such phenomenon also explains well why DTCs outgrown in the first metastatic site can reenter the circulation and colonize the second metastatic site [349,350], likely through reversible E-M and M-E plasticity without affecting periFN assembly on their cell surfaces. Aforementioned interchanges of various phenotypes in tumor cells, stromal cells, and stromal FN during the whole processes of tumor genetic/epigenetic evolution and progression where hypoxia and PMN are critically at the crossroads are illustrated in Figure 4.…”

Section: Malignant Tumor Cells In the Primary Tissues Early Establishmentioning

confidence: 98%

Fibronectin in Cancer: Friend or Foe

Lin

Yang

et al. 2019

Cells

147

117

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The role of fibronectin (FN) in tumorigenesis and malignant progression has been highly controversial. Cancerous FN plays a tumor-suppressive role, whereas it is pro-metastatic and associated with poor prognosis. Interestingly, FN matrix deposited in the tumor microenvironments (TMEs) promotes tumor progression but is paradoxically related to a better prognosis. Here, we justify how FN impacts tumor transformation and subsequently metastatic progression. Next, we try to reconcile and rationalize the seemingly conflicting roles of FN in cancer and TMEs. Finally, we propose future perspectives for potential FN-based therapeutic strategies. Figure 1. (A) The structure of fibronectin (FN) containing three types of repeats and three alternative splicing regions (EDA, EDB, and IIICS) with several well-known binding sites for extracellular matrix (ECM) components (fibrin, heparin, collagen, and gelatin), polymeric assembly (FN-FN), cell adhesion (integrin α5β1), DPP IV, and two C-terminal disulfide bonds for dimeric FN. (B) Publications in recent some forty years regarding the roles of cancerous FN and stromal FN in ECM in tumor progression as represented in a time-line pattern. Among 26 publications before 2000, 15 (57.7%) papers are related to the role of cancerous FN in tumor suppression (in light green boxes), 3 (11.5%) papers are related to the role of cancerous FN in metastasis promotion (in orange boxes), and 8 (30.8%) papers are related to the role of stromal FN in promoting early tumor progression but not late metastasis (in dark green boxes). On the contrary, Among 46 publications after 2000, 7 (15.2%) papers are related to the role of cancerous FN in tumor suppression (in light green boxes), 25 (54.4%) papers are related to the role of cancerous FN in metastasis promotion (in orange boxes), and 14 (30.4%) papers are related to the role of stromal FN in promoting early tumor progression but not late metastasis (in dark green boxes). Abbreviations in boxes are referred to the context of this article. (C) Percentages of articles for the three various roles of FN (the same colors as depicted in (B) before 2000 and after 2000. Numbers in the parenthesis represent article numbers. The Pathobiology of CancerFigure 1. (A) The structure of fibronectin (FN) containing three types of repeats and three alternative splicing regions (EDA, EDB, and IIICS) with several well-known binding sites for extracellular matrix (ECM) components (fibrin, heparin, collagen, and gelatin), polymeric assembly (FN-FN), cell adhesion (integrin α5β1), DPP IV, and two C-terminal disulfide bonds for dimeric FN. (B) Publications in recent some forty years regarding the roles of cancerous FN and stromal FN in ECM in tumor progression as represented in a time-line pattern. Among 26 publications before 2000, 15 (57.7%) papers are related to the role of cancerous FN in tumor suppression (in light green boxes), 3 (11.5%) papers are related to the role of cancerous FN in metastasis promotion (in orange boxes), and 8 (30.8%) papers are related to the r...

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Section: Malignant Tumor Cells In the Primary Tissues Early Establishmentioning

confidence: 98%

Fibronectin in Cancer: Friend or Foe

Lin

Yang

et al. 2019

Cells

147

117

View full text Add to dashboard Cite

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“…Vascular cell adhesion molecule-1 (VCAM-1) is aberrantly expressed in breast cancer cells and binds to a4b1 integrin, which also interacts with fibronectin and is expressed in natural killer cells, monocytes, and other immune cells. 131 It was shown that the pulmonary parenchyma containing collagen and elastin fibers acts as a preferable soil for the homing of VCAM-1-expressing breast cancer. 132 …”

Section: Extracellular Matrix (Ecm) Proteinsmentioning

confidence: 99%

Breast cancer lung metastasis: Molecular biology and therapeutic implications

Jin

Han

Siegel

et al. 2018

Cancer Biology & Therapy

228

164

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Distant metastasis accounts for the vast majority of deaths in patients with cancer. Breast cancer exhibits a distinct metastatic pattern commonly involving bone, liver, lung, and brain. Breast cancer can be divided into different subtypes based on gene expression profiles, and different breast cancer subtypes show preference to distinct organ sites of metastasis. Luminal breast tumors tend to metastasize to bone while basal-like breast cancer (BLBC) displays a lung tropism of metastasis. However, the mechanisms underlying this organ-specific pattern of metastasis still remain to be elucidated. In this review, we will summarize the recent advances regarding the molecular signaling pathways as well as the therapeutic strategies for treating breast cancer lung metastasis.

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“…Cancer metastasis is one of the major causes of cancer‐related deaths . During metastasis, primary tumor cells migrate from the parent tumor into neighboring tissues to form secondary tumors .…”

Section: Introductionmentioning

confidence: 99%

Metastatic cancer cell attachment to endothelium is promoted by endothelial glycocalyx sialic acid degradation

et al. 2019

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While it is known that cancer cell interactions with vascular endothelial cells (ECs) drive metastatic cancer cell extravasation from blood vessels into secondary tumor sites, the mechanisms of action are still poorly understood. Here, we tested the hypothesis that neuraminidase‐induced degradation of EC surface glycocalyx (GCX), particularly the sialic acid (SA) residue components of the GCX, will substantially increase metastatic cancer cell attachment to ECs. To our knowledge, our study is the first to isolate the role of GCX SA residues in cancer cell attachment to the endothelium, which were found to be differentially affected by the presence of neuraminidase and to indeed regulate metastatic cancer cell homing to ECs. We hope that this work will eventually translate to identification of EC GCX‐based cancer markers that can be therapeutically targeted to hinder the progression of metastasis.

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Breast cancer metastasis: Putative therapeutic role of vascular cell adhesion molecule-1

Cited by 112 publications

References 73 publications

Fibronectin in Cancer: Friend or Foe

Fibronectin in Cancer: Friend or Foe

Breast cancer lung metastasis: Molecular biology and therapeutic implications

Metastatic cancer cell attachment to endothelium is promoted by endothelial glycocalyx sialic acid degradation

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