HGF-MET as a breast cancer biomarker

Liu, Shuying

doi:10.18632/aging.100735

Cited by 9 publications

(9 citation statements)

References 7 publications

(10 reference statements)

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“…In malignant tumors, HGF is primarily expressed and released by surrounding stromal cells, including CAFs and TAMs [ 16 , 55 ]. However, HGF can also be produced by several tumor cell types and is detected in the renal cell [ 56 ], colorectal [ 57 , 58 ] and breast carcinomas [ 59 , 60 ], glioma [ 61 ], multiple myeloma [ 62 ] and synovial [ 63 ], osteo- and fibrosarcoma [ 38 ]. On the other hand, the c-MET receptor is overexpressed in several solid tumors, such as medulloblastoma [ 64 ], lymphoma [ 65 ], melanoma [ 66 ], glioma [ 67 ], breast [ 68 ], pancreatic [ 69 ], colorectal, ovarian and prostate carcinomas, as well as osteo- and some soft-tissue sarcomas [ 38 ].…”

Section: Hgf/c-met Signaling Pathway Mediates Cancer Progressionmentioning

confidence: 99%

Extracellular Matrix Influencing HGF/c-MET Signaling Pathway: Impact on Cancer Progression

Noriega-Guerra

Freitas

2018

IJMS

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The extracellular matrix (ECM) is a crucial component of the tumor microenvironment involved in numerous cellular processes that contribute to cancer progression. It is acknowledged that tumor–stromal cell communication is driven by a complex and dynamic network of cytokines, growth factors and proteases. Thus, the ECM works as a reservoir for bioactive molecules that modulate tumor cell behavior. The hepatocyte growth factor (HGF) produced by tumor and stromal cells acts as a multifunctional cytokine and activates the c-MET receptor, which is expressed in different tumor cell types. The HGF/c-MET signaling pathway is associated with several cellular processes, such as proliferation, survival, motility, angiogenesis, invasion and metastasis. Moreover, c-MET activation can be promoted by several ECM components, including proteoglycans and glycoproteins that act as bridging molecules and/or signal co-receptors. In contrast, c-MET activation can be inhibited by proteoglycans, matricellular proteins and/or proteases that bind and sequester HGF away from the cell surface. Therefore, understanding the effects of ECM components on HGF and c-MET may provide opportunities for novel therapeutic strategies. Here, we give a short overview of how certain ECM components regulate the distribution and activation of HGF and c-MET.

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Section: Hgf/c-met Signaling Pathway Mediates Cancer Progressionmentioning

confidence: 99%

Extracellular Matrix Influencing HGF/c-MET Signaling Pathway: Impact on Cancer Progression

Noriega-Guerra

Freitas

2018

IJMS

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“…MSCs migrate towards breast cancer cells via hypoxia-induced interleukin 6 (IL6) secretion [ 47 ] and towards primary breast tumors via the hypoxia-inducible factor alpha (HIFα)-dependent secretion of CXCL16 [ 48 ]. Hypoxia-induced hepatocyte growth factor (HGF) may also mediate recruitment [ 49 ] as it is upregulated in serum of breast cancer patients [ 50 , 51 ] and associated with tumor formation and metastasis in breast [ 52 , 53 ] and prostate cancer [ 54 ]. Furthermore, the activation of HGF receptor, MET, in bone marrow stromal cells by melanoma cells is associated with metastasis [ 55 ].…”

Section: Mesenchymal Stromal Cells Within the Tumor Microenvironmementioning

confidence: 99%

Mesenchymal Stromal Cells: Emerging Roles in Bone Metastasis

Graham

Qian²

2018

IJMS

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Bone metastasis is the most advanced stage of many cancers and indicates a poor prognosis for patients due to resistance to anti-tumor therapies. The establishment of metastasis within the bone is a multistep process. To ensure survival within the bone marrow, tumor cells must initially colonize a niche in which they can enter dormancy. Subsequently, reactivation permits the proliferation and growth of the tumor cells, giving rise to a macro-metastasis displayed clinically as a bone metastatic lesion. Here, we review the evidences that suggest mesenchymal stromal cells play an important role in each of these steps throughout the development of bone metastasis. Similarities between the molecular mechanisms implicated in these processes and those involved in the homeostasis of the bone indicate that the metastatic cells may exploit the homeostatic processes to their own advantage. Identifying the molecular interactions between the mesenchymal stromal cells and tumor cells that promote tumor development may offer insight into potential therapeutic targets that could be utilized to treat bone metastasis.

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“…Currently, many targeted approaches to cancer therapy have focused on the reliance of cancer cells on HGF/MET signaling for cell proliferation. Although approaches targeting MET, for instance diverse specific MET inhibitors, monoclonal antibodies and siMET, were developed, and have yielded promising results in preclinical studies, few clinical trials of MET inhibitors have demonstrated the expected therapeutic benefits [7]. This inconsistency raises the possibilities that there are different regulatory mechanisms of HGF/MET signaling in different cancers.…”

mentioning

confidence: 99%