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HTR3A is correlated with the unfavorable histology and promotes proliferation via ERK phosphorylation in lung adenocarcinoma

ABSTRACT: HTR3A is correlated with the unfavorable histology and promotes proliferation via ERK phosphorylation in lung adenocarcinoma

PROVIDER: PRJNA625748 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11557566.fastq.gz	Fastqsanger.gz
	SRR11557567.fastq.gz	Fastqsanger.gz
	SRR11557568.fastq.gz	Fastqsanger.gz
	SRR11557569.fastq.gz	Fastqsanger.gz
	SRR11557570.fastq.gz	Fastqsanger.gz

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Project description:Lung cancer is the leading cause of cancer death around the world. Adenocarcinoma is the most common histological type and has various histologic subtypes: lepidic, acinar, papillary, solid, and invasive mucinous adenocarcinoma. Histologic subtypes are related to invasiveness of tumors; for example, lepidic subtype is less invasive than acinar/papillary subtype. HTR3A is the main subunit of 5-hydroxytryptamine 3 (5-HT3) receptors, which are the only ligand-gated ion channels in 7 families of 5-HT receptors. Though 5-HT3 receptor is expressed mainly throughout the central and peripheral nervous systems, some papers report the effect of 5-HT3 receptors on tumor cells including lung cancer. However, whether HTR3A correlates with histopathological findings such as the histologic subtypes or the distribution in an individual sample remains unclear. Immunohistochemically, we revealed, the higher expression level of HTR3A was detected in acinar, papillary, and solid adenocarcinoma than in lepidic adenocarcinoma; the former was more aggressive subtype than the latter. We also showed the relationship between the expression of HTR3A and Ki-67, widely used as a proliferation marker. Moreover, we generated HTR3A-knockdown lung adenocarcinoma cells and showed that the HTR3A knockdown attenuated proliferation via ERK phosphorylation. Our results demonstrated that HTR3A expression was related to proliferation in lung adenocarcinoma by means of both in vitro and immunohistochemical assays on clinical samples. We showed the therapeutic potential of a 5-HT3 receptor antagonist, tropisetron, for the treatment of lung adenocarcinoma.

2020-08-03 | GSE148801 | GEO

Project description:Lung cancer is the leading cause of cancer death around the world. Adenocarcinoma is the most common histological type and has various histologic subtypes: lepidic, acinar, papillary, solid, and invasive mucinous adenocarcinoma. Histologic subtypes are related to invasiveness of tumors; eg, lepidic subtype is less invasive than acinar/papillary subtype. HTR3A is the main subunit of 5-hydroxytryptamine 3 (5-HT3) receptors, which are the only ligand-gated ion channels in seven families of 5-HT receptors. Although 5-HT3 receptor is expressed mainly throughout the central and peripheral nervous systems, some papers report the effect of 5-HT3 receptors on tumor cells, including lung cancer. However, whether HTR3A correlates with histopathological findings such as the histologic subtypes or the distribution in an individual sample remains unclear. Immunohistochemically, we revealed that the higher expression level of HTR3A was detected in acinar, papillary, and solid adenocarcinoma than in adenocarcinoma in situ and lepidic adenocarcinoma; the former was a more aggressive subtype than the latter. We also showed the relationship between HTR3A expression and Ki-67 positivity, widely used as a proliferation marker. Moreover, we generated HTR3A-knockdown lung adenocarcinoma cells and showed that the HTR3A knockdown attenuated proliferation by ERK phosphorylation. Our results indicated that HTR3A expression was related to proliferation in lung adenocarcinoma, by means of both in vitro and immunohistochemical assays on clinical samples. We showed the therapeutic potential of a 5-HT3 receptor antagonist, tropisetron, for the treatment of lung adenocarcinoma.

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Impact of Genomic and Clinical Factors on Outcome of Children ≥18 Months of Age with INSS Stage 3 Neuroblastoma with Unfavorable Histology without MYCN Amplification

Project description:Patients with INSS stage 3, MYCN–non-amplified, unfavorable histology neuroblastoma represent a rare subset of children with outcomes that are inferior to those of most patients with advanced locoregional disease, and superior to those of most high-risk patients. We evaluated the impact of clinical variables on outcome and used available tumor samples from subjects within this subgroup to correlate whole exome sequencing (WES) and RNA sequencing (RNASeq) profiles with outcome. We found that subjects with tumors harboring chromosome 11q losses had inferior outcomes and describe an expression profile with universally favorable outcomes. These findings provide a framework for a refined risk stratification where patients with 11q loss could be included with traditional high-risk groups and patients with a favorable expression profile could be considered to have non-high-risk disease.

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As an unfavorable prognostic factor, LACTB promotes metastasis of nasopharyngeal carcinoma via activation of ERBB3/EGFR-ERK signaling

Project description:As an unfavorable prognostic factor, LACTB promotes metastasis of nasopharyngeal carcinoma via activation of ERBB3/EGFR-ERK signaling

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As an unfavorable prognostic factor, LACTB promotes metastasis of nasopharyngeal carcinoma via activation of ERBB3/EGFR-ERK signaling

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Project description:Deregulated cell migration and invasion, which are hallmarks of metastatic cancer cells, are correlated to structural and functional alterations of the actin cytoskeleton associated to a large panel of actin-binding proteins. Among these, the actin-bundling protein L-plastin, initially detected in leukocytes, is ectopically expressed in several solid tumours and is often considered as a metastatic marker. Phosphorylation of L-plastin on residue serine 5 (Ser5) has been shown to activate L-plastin and to be crucial for invasion and metastasis formation. Here, we investigate the signalling pathway leading to L-plastin Ser5 phosphorylation in four breast cancer cell lines. Whole genome microarray analysis comparing cell lines with different invasive capacities and corresponding L-plastin Ser5 phosphorylation levels revealed that genes of the MAPK/ERK pathway are differentially expressed. In line, in vitro kinase assays showed that MAPK/ERK pathway downstream kinases RSK1 and RSK2 are able to directly phosphorylate L-plastin on Ser5. In parallel to a knockdown approach, activation and inhibition studies of signalling molecules of the MAPK/ERK pathway, followed by computational modelling analysis, confirmed that RSK is an important activator of L-plastin in all four studied cell lines. Finally and rounding up our study, RSK knockdown significantly impaired migratory and invasive capacities of a selected invasive cell line, thus consolidating RSK as a promising therapeutic target in certain invasive carcinomas. Altogether, our data provide substantial evidence that the MAPK/ERK pathway is involved in L-plastin Ser5 phosphorylation in breast cancer cells with its downstream kinases RSK1 and RSK2 being able to directly phosphorylate L-plastin on Ser5.

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