Collapsin response mediator proteins: Potential diagnostic and prognostic biomarkers in cancers (Review)

Tan, Fei; Thiele, Carol J.; Li, Zhijie

doi:10.3892/ol.2014.1909

Cited by 35 publications

(43 citation statements)

References 58 publications

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“…Most studies of CRMP focus on its role in axonal guidance in the developing nervous system and CRMP has been show highly expressed in the developing and injured nervous system (1), however, recent study indicated that CRMP is involved in several malignant diseases (12). Shih et al reported that CRMP1 negatively correlated with lung cancer invasiveness (13), further study indicated LCRMP1, a long form isoform of CRMP1, promotes lung cancer cell invasiveness and this effect may relate to LCRMP1-WAVE1 combination and GSK-3β phosphorylation of LCRMP1 (14,15).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of CRMP4, a new prostate cancer metastasis suppressor gene, inhibits tumor growth in a nude mouse intratibial injection model

Zhou

Xie

Pang

et al. 2014

International Journal of Oncology

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Prostate cancer, the most commonly diagnosed male cancer in North America, has a high incidence of bone metastasis. Our previous study showed collapsin response mediator protein 4 (CRMP4) gene inhibited prostate cancer migration and invasion. In this study, we investigated whether overexpression of CRMP4 gene in prostate cancer cells inhibit tumor bone metastasis. The stable prostate cancer cells overexpressing the CRMP4 gene were constructed using lentivirus infection. Prostate cancer bone metastasis nude mouse model was built though orthotopic prostate implantation, intracardiac injection and intratibial injection with CRMP4 overexpress and control cancer cells. Small animal PET/CT scanning results showed no difference of bone metastatic capacity in orthotopic and intracardiac injection models between CRMP4 overexpression and control group, while CRMP4 overexpression inhibited tumor growth in the intratibial injection model. Moreover, our in vitro study showed CRMP4 overexpression downregulates the Neuropilin1 (NRP1) expression and upregulate the Noggin expression. Immunohistochemical staining of the hind limbs of intratibial injection model was confirmed with cytological experiments. Taken together, our research indicated CRMP4 inhibits prostate cancer cells growth in the nude mouse bone microenvironment and this effect may relate with regulation of NRP1 and Noggin expression.

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Section: Introductionmentioning

confidence: 99%

Upregulation of CRMP4, a new prostate cancer metastasis suppressor gene, inhibits tumor growth in a nude mouse intratibial injection model

Zhou

Xie

Pang

et al. 2014

International Journal of Oncology

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“…Altered CRMP levels where detected in several cancers, including breast, colorectal, prostate, pancreatic, and neuroendocrine lung carcinoma (6). CRMPs are found broadly expressed within tissues and the understanding of their cellular functions is expanding.…”

Section: Introductionmentioning

confidence: 99%

CRMP5 Controls Glioblastoma Cell Proliferation and Survival through Notch-Dependent Signaling

et al. 2015

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Collapsin response mediator protein 5 (CRMP5) belongs to a family of five cytosolic proteins that play a major role in nervous system development. This protein was first described in cancerinduced autoimmune processes, causing neurodegenerative disorders (paraneoplastic neurologic syndromes). CRMP5 expression has been reported to serve as a biomarker for high-grade lung neuroendocrine carcinomas; however, its functional roles have not been examined in any setting of cancer pathophysiology. In this study, we report two different CRMP5 expression patterns observed in human glioblastoma (GBM) biopsies that establish connections between CRMP5 expression, Notch receptor signaling, and GBM cell proliferation. We demonstrated that elevated CRMP5 promotes Notch receptor expression and Akt activation in human tumor cell lines, GBM stem cells, and primary tumor biopsies. We have shown that the high CRMP5 and Notch expression in GBM xenograft is related to stem cells. This suggests that high CRMP5 expression pattern in GBM biopsies encompasses a subset of stem cells. Mechanistically, CRMP5 functioned by hijacking Notch receptors from Itch-dependent lysosomal degradation. Our findings suggest that CRMP5 serves as a major mediator of Notch signaling and Akt activation by controlling the degradation of the Notch receptor, with implications for defining a biomarker signature in GBM that correlates with and may predict patient survival. Cancer Res; 75(17); 3519-28. Ó2015 AACR.

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“…Moreover, the CRMPs that are low in expression in the intact adult nervous system was found to have increased expression in the disease models, and its expression has also been confirmed in non-neuronal cells, such as cancer cells [37], T cells [38][39][40], and glial cells [41][42][43]. The expression and functions of CRMPs (but not CRMP3) have been well demonstrated in the lung, breast, pancreatic, and prostate cancerous tissues.…”

Section: Homology and Heterogeneity Of Crmpsmentioning

confidence: 85%

“…The expression and functions of CRMPs (but not CRMP3) have been well demonstrated in the lung, breast, pancreatic, and prostate cancerous tissues. Each CRMP and its splicing variant have distinct roles in cancer progression and metastasis, suggesting their therapeutic potential (see review [37]). In this review, we would like to discuss the emerging roles of CRMPs in T cells and glial cells.…”

Section: Homology and Heterogeneity Of Crmpsmentioning

confidence: 99%

“…Several studies have indicated that CRMPs serve a diverse and significant role for bone formation [131,132], cancer progression, and metastasis [37]. In particular, paraneoplastic IgG autoantibodies specific to CRMP-5 from patients [139] provides the possibility to reveal the mechanisms of paraneoplastic neurologic disorders.…”

Section: Conclusion and Future Outlookmentioning

confidence: 99%

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CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury

2016

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Neurodegeneration in the adult mammalian central nervous system (CNS) is fundamentally accelerated by its intrinsic neuronal mechanisms, including its poor regenerative capacity and potent extrinsic inhibitory factors. Thus, the treatment of neurodegenerative diseases faces many obstacles. The degenerative processes, consisting of axonal/dendritic structural disruption, abnormal axonal transport, release of extracellular factors, and inflammation, are often controlled by the cytoskeleton. From this perspective, regulators of the cytoskeleton could potentially be a therapeutic target for neurodegenerative diseases and CNS injury. Collapsin response mediator proteins (CRMPs) are known to regulate the assembly of cytoskeletal proteins in neurons, as well as control axonal growth and neural circuit formation. Recent studies have provided some novel insights into the roles of CRMPs in several inhibitory signaling pathways of neurodegeneration, in addition to its functions in neurological disorders and CNS repair. Here, we summarize the roles of CRMPs in axon regeneration and its emerging functions in non-neuronal cells, especially in inflammatory responses. We also discuss the direct and indirect targeting of CRMPs as a novel therapeutic strategy for neurological diseases.

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Collapsin response mediator proteins: Potential diagnostic and prognostic biomarkers in cancers (Review)

Cited by 35 publications

References 58 publications

Upregulation of CRMP4, a new prostate cancer metastasis suppressor gene, inhibits tumor growth in a nude mouse intratibial injection model

Upregulation of CRMP4, a new prostate cancer metastasis suppressor gene, inhibits tumor growth in a nude mouse intratibial injection model

CRMP5 Controls Glioblastoma Cell Proliferation and Survival through Notch-Dependent Signaling

CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury

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