NeuroD1 mediates nicotine-induced migration and invasion via regulation of the nicotinic acetylcholine receptor subunits in a subset of neural and neuroendocrine carcinomas

Osborne, Jihan K.; Guerra, Marcy L.; Gonzales, Joshua X.; McMillan, Elizabeth A.; Minna, John D.; Cobb, Melanie H.

doi:10.1091/mbc.e13-06-0316

Cited by 16 publications

(13 citation statements)

References 71 publications

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“…Based on pro‐inflammatory effects of macrophages and on cancer growth exerted by MIF which suppresses the function of p53 [Bifulco et al, ], one could reason that the MIF‐driven cancer cell proliferation, invasiveness, and metastasis in response to IR observed in our study were due to suppressed p53 activity. However, A549 cells contain wild‐type p53 while NCI‐H358 cells lack expression of p53 [Kasiappan et al, ; Osborne et al, ]. Similar results from the two cell lines in almost all of our experiments suggest that p53 was not associated with the results of the present study.…”

Section: Discussionsupporting

confidence: 79%

Dissociation of MIF‐rpS3 Complex and Sequential NF‐κB Activation Is Involved in IR‐Induced Metastatic Conversion of NSCLC

Youn

Son

Kim

et al. 2015

J of Cellular Biochemistry

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Frequent relapse and spreading of tumors during radiotherapy are principal obstacles to treatment of non-small cell lung cancer (NSCLC). In this study, we aimed to investigate how macrophage migration inhibitory factor (MIF) which is expressed at high levels in metastatic and primary lung cancer cells could regulate NSCLC metastasis in response to ionizing radiation (IR). The results indicated that MIF and ribosomal protein S3 (rpS3) were shown to be connected to inflammation, proliferation, and metastasis of NSCLC via IR-induced activation of the NF-κB pathway. Under unirradiated conditions, MIF physically established a complex with rpS3. MIF-rpS3 dissociation induced by IR activated NF-κB and made the expression of target genes of this factor transactivated in two NSCLC cell lines, A549, and NCI-H358. We also found that IR-induced dissociation of this complex led to increased secretion of pro-inflammatory cytokines and modulated the expression of epithelial-mesenchymal transition marker proteins. Finally, the effects of IR-induced dissociation of the MIF-rpS3 complex on tumor metastasis were confirmed by in vivo xenograft studies. Taken together, the present study revealed that dissociation of the MIF-rpS3 complex and subsequent activation of NF-κB is a critical post-IR exposure event that accounts for IR-induced metastatic conversion of NSCLC.

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Section: Discussionsupporting

confidence: 79%

Dissociation of MIF‐rpS3 Complex and Sequential NF‐κB Activation Is Involved in IR‐Induced Metastatic Conversion of NSCLC

Youn

Son

Kim

et al. 2015

J of Cellular Biochemistry

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“…However, the variants p.G1504=, p.S1535P and the intronic c.652-6del of COL11A1, and the intronic polymorphism c.6068 + 5249A > T of DOCK8 were maintained with the same allelic frequency (nearly 1) in all the samples. SH-SY5Y cell lines grown in 2D, as well as in 3D hydrogels and mice, showed the pathogenic mutation described as p.F1174L in ALK [47], as well as p.G12V in KRAS not previously reported in this cell line [48]. We did not nd any new signi cant mutations (Table S2).…”

Section: Biotensegrity Had Impact In Single Nucleotide Mutationssupporting

confidence: 55%

Impact of extracellular matrix properties on neuroblastoma genomic heterogeneity

López-Carrasco¹,

Martín-Vañó²,

Burgos‐Panadero³

et al. 2020

Preprint

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Background Increased tissue stiffness is a common feature of malignant solid tumors, often associated with metastasis and poor patient outcomes. Vitronectin, as an extracellular matrix anchorage glycoprotein related to a stiff matrix, is present in a particularly increased quantity and specific distribution in high-risk neuroblastoma. Furthermore, as cells can sense and transform the proprieties of the extracellular matrix into chemical signals through mechanotransduction, genotypic changes related to stiffness are possible. Methods We have applied high density SNPa and NGS techniques to in vivo and in vitro models (orthotropic xenograft vitronectin knock-out mice and 3D bioprinted hydrogels with different stiffness) using two representative neuroblastoma cell lines (the MYCN amplified SK-N-BE(2) and the ALK mutated SH-SY5Y), to discern how tumor genomics patterns and clonal heterogeneity of both cell lines are affected. Results We describe a remarkable subclonal selection of some genomic aberrations in SK-N-BE(2) cells grown in knock-out vitronectin xenograft mice that also emerged when cultured for long times in stiff hydrogels. Specially, we detected an enlarged subclonal cell population with chromosome 9 aberrations in both models. Similar abnormalities were found in human high-risk neuroblastoma with MYCN amplification. Genomics of the SH-SY5Y cell line remained stable when cultured in both models. Conclusions Focus on heterogeneous intratumor segmental chromosome aberrations and mutations, as a mirror image of tumor microenvironment, is a vital area of future research.

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“…However, the variants p.G1504=, p.S1535P and the intronic c.652-6del of COL11A1, and the intronic polymorphism c.6068+5249A>T of DOCK8 were maintained with the same allelic frequency (nearly 1) in all the samples. SH-SY5Y cell lines grown in 2D, as well as in 3D hydrogels and mice, showed the pathogenic mutation described as p.F1174L in ALK [47], as well as p.G12V in KRAS not previously reported in this cell line [48]. We did not nd any new signi cant mutations (Table S2).…”

Section: Biotensegrity Had Impact In Single Nucleotide Mutationssupporting

confidence: 53%

Impact of extracellular matrix stiffness on genomic heterogeneity in MYCN-amplified neuroblastoma cell line

López-Carrasco

Martín-Vañó

Burgos‐Panadero

et al. 2020

Preprint

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Background: Increased tissue stiffness is a common feature of malignant solid tumors, often associated with metastasis and poor patient outcomes. Vitronectin, as an extracellular matrix anchorage glycoprotein related to a stiff matrix, is present in a particularly increased quantity and specific distribution in high-risk neuroblastoma. Furthermore, as cells can sense and transform the proprieties of the extracellular matrix into chemical signals through mechanotransduction, genotypic changes related to stiffness are possible.Methods: We applied high density SNPa and NGS techniques to in vivo and in vitro models (orthotropic xenograft vitronectin knock-out mice and 3D bioprinted hydrogels with different stiffness) using two representative neuroblastoma cell lines (the MYCN-amplified SK-N-BE(2) and the ALK -mutated SH-SY5Y), to discern how tumor genomics patterns and clonal heterogeneity of the two cell lines are affected. Results: We describe a remarkable subclonal selection of genomic aberrations in SK-N-BE(2) cells grown in knock-out vitronectin xenograft mice that also emerged when cultured for long times in stiff hydrogels. In particular, we detected an enlarged subclonal cell population with chromosome 9 aberrations in both models. Similar abnormalities were found in human high-risk neuroblastoma with MYCN amplification. The genomics of the SH-SY5Y cell line remained stable when cultured in both models. Conclusions: Focus on heterogeneous intratumor segmental chromosome aberrations and mutations, as a mirror image of tumor microenvironment, is a vital area of future research.

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NeuroD1 mediates nicotine-induced migration and invasion via regulation of the nicotinic acetylcholine receptor subunits in a subset of neural and neuroendocrine carcinomas

Cited by 16 publications

References 71 publications

Dissociation of MIF‐rpS3 Complex and Sequential NF‐κB Activation Is Involved in IR‐Induced Metastatic Conversion of NSCLC

Dissociation of MIF‐rpS3 Complex and Sequential NF‐κB Activation Is Involved in IR‐Induced Metastatic Conversion of NSCLC

Impact of extracellular matrix properties on neuroblastoma genomic heterogeneity

Impact of extracellular matrix stiffness on genomic heterogeneity in MYCN-amplified neuroblastoma cell line

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