Functions of chemokines in the perineural invasion of tumors (Review)

Zhang, Mei; Zhu, Zhuo-Li; Gao, Xiaolei; Wu, Jian; Liang, Xin‐hua; Tang, Yaling

doi:10.3892/ijo.2018.4311

Cited by 12 publications

(15 citation statements)

References 133 publications

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“…Furthermore, CTSB overexpression was associated with perineural invasion (PNI) in SACC. PNI, a hallmark of SACC, is an independent indicator of tumor recurrence and a poor prognosis ( 44 - 46 ). The role of cathepsins in PNI of SACC was also demonstrated in our previous study, in which cathepsin D was overexpressed in the nerve invasion frontier and associated with a poor prognosis of patients with SACC ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

Cathepsin B defines leader cells during the collective invasion of salivary adenoid cystic carcinoma

Wang

et al. 2019

Int J Oncol

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Cathepsin B (CTSB) has been reported to be involved in cancer metastasis by altering extracellular matrix (ECM) remodeling and facilitating invasion. However, the contribution of CTSB to collective cell invasion in salivary adenoid cystic carcinoma (SACC) and the underlying mechanisms remain unclear. The present study demonstrated that collective cell invasion is commonly observed in SACC without a complete epithelial-mesenchymal transition signature. CTSB was found to be overexpressed in the invasive front of SACC compared to the tumor center, and was associated with a poor prognosis of patients with SACC. Subsequently, a 3D spheroid invasion assay was established in order to recapitulate the collective cell invasion of SACC and the results revealed that CTSB was only expressed in leader cells. The knockdown of CTSB by siRNA inhibited the migration and invasion of SACC-83 cells and impaired the formation of leader cells. CTSB knockdown also disrupted cytoskeletal organization, altered cell morphology and inhibited ECM remodeling by downregulating matrix metalloproteinase-9, focal adhesion kinase and Rho/ROCK function. Therefore, the present study provides evidence that CTSB may define leader cells in SACC and is required for collective cell invasion as a potential key regulator of ECM remodeling.

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Section: Discussionmentioning

confidence: 99%

Cathepsin B defines leader cells during the collective invasion of salivary adenoid cystic carcinoma

Wang

et al. 2019

Int J Oncol

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“…CX3CL1 (C-X3-C Motif Chemokine Ligand 1) is found to be abundantly produced and released by neurons. An elevated expression level of its receptor, CX3CR1 (C-X3-C Motif Chemokine receptor 1), has been implicated in the development of PNI and earlier recurrence of numerous cancers, such as PC, gastric cancer, and prostate cancer ( 68 – 70 ). Equally important, both in vitro co-culture and in vivo PNI models demonstrated that nerve cells, including Schwann cells and neurons, express CCL2 (C-C motif chemokine ligand 2) which capable of inducinge the migration of CCR2 (C-C Motif Chemokine receptor 2) expressing cancer cells toward these nerves, ultimately promoting PNI progression ( 16 , 71 , 72 ).…”

Section: The Perineural Niche and Tumor Microenvironment In Pnimentioning

confidence: 99%

Perineural Invasion in Adenoid Cystic Carcinoma of the Salivary Glands: Where We Are and Where We Need to Go

et al. 2020

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Adenoid cystic carcinoma of the salivary gland (SACC) is a rare malignant tumors of the head and neck region, but it is one of the most common malignant tumors that are prone to perineural invasion (PNI) of the head and neck. The prognosis of patients with SACC is strongly associated with the presence of perineural spread (PNS). Although many contributing factors have been reported, the mechanisms underlying the preferential destruction of the blood-nerve barrier (BNB) by tumors and the infiltration of the tumor microenvironment by nerve fibers in SACC, have received little research attention. This review summarizes the current knowledge concerning the characteristics of SACC in relation to the PNI, and then highlights the interplay between components of the tumor microenvironment and perineural niche, as well as their contributions to the PNI. Finally, we provide new insights into the possible mechanisms underlying the pathogenesis of PNI, with particular emphasis on the role of extracellular vesicles that may serve as an attractive entry point in future studies.

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“…9 They have chemotaxis and activation effects on monocytes, lymphocytes and neutrophils. 15,16 Chemokines are highly homologous and can be classified into C, CC, CXC and CX3C subtypes. IP10 is a chemokine screened from U937 cells and it is also named CXCL10.…”

Section: Discussionmentioning

confidence: 99%

<p>IP10-CDR3 Reduces The Viability And Induces The Apoptosis Of Ovarian Cancer Cells By Down-Regulating The Expression Of Bcl-2 And Caspase 3</p>

Chen

Zhuang

et al. 2019

OTT

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This study aimed to explore the effects of interferon-γ inducible protein 10 (IP10) and complementarity-determining region 3 (CDR3) of T cells receptor on ovarian cancer cells and the involved mechanisms. Methods: IP10 and CDR3 were linked with single-chain antibody (scfv) and exotoxin gene muton of Pseudomonas aeruginosa (PE40) to construct IP10-CDR3scfv and IP10-CDR3-PE40scfv. Then, we constructed pcDNA3.1-IP10-CDR3scfv and pcDNA3.1-IP10-CDR3-PE40scfv plasmids which were proved by HindIII/EcoRI digestion. SKOV3 cells and HOSEpiC cells were incubated with fluorescein isothiocyanate (FITC) labeled IP10-CDR3scfv and IP10-CDR3-PE40scfv proteins and protein levels were examined by flow cytometry. After gene transfection, SKOV3 cells were divided into four groups: Control, pcDNA3.1(+) negative control (NC) (pcDNA3.1(+) NC transfection), IP10-CDR3scfv (IP10-CDR3scfv transfection) and IP10-CDR3-PE40scfv (IP10-CDR3-PE40scfv transfection). Levels of IP10, CDR3, Caspase-3, cleaved Caspase-3 and Bcl-2 were determined by RT-PCR and Western blot. Cell viability and apoptosis were investigated by CCK-8 assay and Annexin V-FITC/PI assay, respectively. Results: The levels of FITC-labeled IP10-CDR3scfv and IP10-CDR3-PE40scfv proteins in the SKOV3+IP10-CDR3scfv group and the SKOV3+IP10-CDR3-PE40scfv group were remarkably higher than that in the SKOV3 group (P<0.05). So was the HOSEpiC related groups. There was no obvious difference in the levels of IP10, CDR3, Caspase-3, cleaved Caspase-3 and Bcl-2 between the control group and the pcDNA3.1(+) NC group. However, compared with the control group, the levels of Caspase-3 and Bcl-2 were reduced notably and the levels of IP10, CDR3 and cleaved Caspase-3 were elevated sharply in the IP10-CDR3scfv and IP10-CDR3-PE40scfv groups (P<0.05). The control group and the pcDNA3.1 (+) NC group demonstrated similar cell viability and apoptosis. However, compared with the control group, cell viability in the IP10-CDR3scfv and IP10-CDR3-PE40scfv groups decreased significantly and cell apoptosis increased (P<0.05). Conclusion: IP10-CDR3 could reduce the viability and induce the apoptosis of ovarian cancer cells by down-regulating the expression of Bcl-2 and Caspase-3.

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Functions of chemokines in the perineural invasion of tumors (Review)

Cited by 12 publications

References 133 publications

Cathepsin B defines leader cells during the collective invasion of salivary adenoid cystic carcinoma

Cathepsin B defines leader cells during the collective invasion of salivary adenoid cystic carcinoma

Perineural Invasion in Adenoid Cystic Carcinoma of the Salivary Glands: Where We Are and Where We Need to Go

<p>IP10-CDR3 Reduces The Viability And Induces The Apoptosis Of Ovarian Cancer Cells By Down-Regulating The Expression Of Bcl-2 And Caspase 3</p>

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