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LIS1 promotes perineural invasion by upregulating the serine metabolism in head and neck squamous carcinoma

ABSTRACT: LIS1 is a critical mediator of neuronal migration during brain development, and is strongly associated with malignant tumors. We found that LIS1 is highly expressed in HNSCC,which is releated to perineural infiltration(PNI) in HNSCC.To explore the mechanism of PNI, we silenced the LIS1 expression in HNSCC cells and dected the function of PNI.In a word,We sought to validate LIS1 as a key signaling molecule for PNI in HNSCC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE282822 | GEO | 2025/01/01

REPOSITORIES: GEO

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LIS1 promotes perineural invasion by upregulating the serine metabolism in head and neck squamous carcinoma

Project description:LIS1 promotes perineural invasion by upregulating the serine metabolism in head and neck squamous carcinoma

| PRJNA1190471 | ENA

Expression of microRNAs and Protein-coding Genes Associated with Perineural Invasion in Prostate Cancer

Project description:BACKGROUND. Perineural invasion (PNI) is the dominant pathway for local invasion in prostate cancer. To date, only few studies have investigated the molecular differences between prostate tumors with PNI and those without it. METHODS. To evaluate the involvement of both microRNAs and protein-coding genes in PNI, we determined their genome-wide expression with a custom microRNA microarray and Affymetrix GeneChips in 50 prostate adenocarcinomas with PNI and 7 without it. In-situ hybridization and immunohistochemistry was used to validate candidate genes. RESULTS. Unsupervised classification of the 57 adenocarcinomas revealed two clusters of tumors with distinct global microRNA expression. One cluster contained all non-PNI tumors and a subgroup of PNI tumors. Significance analysis of microarray data yielded a list of microRNAs associated with PNI. At a false discovery rate (FDR) < 10%, 19 microRNAs were higher expressed in PNI tumors than in non-PNI tumors. The most differently expressed microRNA was miR-224. In-situ hybridization showed that this microRNA is expressed by perineural cancer cells. The analysis of protein-coding genes identified 34 transcripts that were differently expressed by PNI status (FDR <10%). These transcripts were down-regulated in PNI tumors. Many of those encoded metallothioneins and proteins with mitochondrial localization and involvement in cell metabolism. Consistent with the microarray data, perineural cancer cells tended to have lower metallothionein expression by immunohistochemistry than nonperineural cancer cells. CONCLUSIONS. Although preliminary, our findings suggest that alterations in microRNA expression, mitochondrial function, and cell metabolism occur at the transition from a non-invasive prostate tumor to a tumor with PNI. Keywords: Disease State analysis

2008-07-01 | GSE7055 | GEO

Gene expression signatures associated with Perineural Invasion in pancreatic ductal adenocarcinoma

Project description:Perineural invasion (PNI) is a prominent characteristic of pancreatic ductal adenocarcinoma (PDAC) and indicates poor prognosis. The invasion of the surrounding nerves by pancreatic cancer cells not only provides route for metastasis but also contributes to neural remodeling and changes in the neuronal milieu that can profoundly influenced the microenvironment of pancreatic cancer. To investigate the downstream molecules associated with PNI, the experiment analyzed mRNA expression of 50 pairs of pancreatic ductal adenocarcinoma tissue and paired adjacent non-tumor tissue, among which 28 pairs of cases diagnosed with PNI by experienced pathologist. Results provide new insight into molecular basis for the influence of PNI on the microenvironment of pancreatic cancer.

2017-08-04 | GSE102238 | GEO

Expression profiling of cutaneous squamous cell carcinoma with perineural invasion implicates the p53 pathway in the process

Project description:Squamous cell carcinoma (SCC) is the second most common cancer worldwide and accounts for approximately 30% of all keratinocyte cancers. The vast majority of cutaneous SCCs of the head and neck (cSCCHN) are readily curable with surgery and/or radiotherapy unless high-risk features are present. Perineural invasion (PNI) is recognized as one of these high-risk features. The molecular changes during clinical PNI in cSCCHN have not been previously investigated. In this study, we assessed the global gene expression differences between cSCCHN with or without incidental or clinical PNI. The results of the analysis showed signatures of gene expression representative of activation of p53 in tumors with PNI compared to tumors without, amongst other alterations. Immunohistochemical staining of p53 showed cSCCHN with clinical PNI to be more likely to exhibit a diffuse over-expression pattern, with no tumors showing normal p53 staining. DNA sequencing of cSCCHN samples with clinical PNI showed no difference in mutation number or position with samples without PNI, however a significant difference was observed in regulators of p53 degradation, stability and activity. Our results therefore suggest that cSCCHN with clinical PNI may be more likely to contain alterations in the p53 pathway, compared to cSCCHN without PNI.

2016-09-08 | GSE86544 | GEO

Transcription profiling of human neuro-invasive pancreatic tumors engineered in-vitro compared to less invasive parental cells

Project description:Perineural invasion (PNI) is considered to be a specific path for the spread of pancreatic cancer cells and PNI is thought to be one of the important factors that determine local recurrence after resection. In addition PNI has been implicated in the pain syndrome that affects the majority of pancreatic ductal adenocarcinoma (PDAC) patients. Here we aimed to investigate the transcriptional differences between neuro-invasive tumors engineered in-vitro compared to less invasive parental cells. Two colour differential hybridisations were performed with human universal reference total RNA (Clontech, #636538).

2009-04-01 | E-TABM-400 | biostudies-arrayexpress

Hepatic loss of Lis1 leads to fatty liver and predisposes to tumorigenesis in mice

Project description:We found that genetic deletion of Lis1 (also known as Pafah1b1) in mouse liver led to increased lipid accumulation and inflammation in the liver. Further analysis revealed that loss of Lis1 led to endoplasmic reticulum (ER) stress and reduced triglyceride secretion. Attenuation of ER stress by tauroursodeoxycholic acid (TUDCA) diminished lipid accumulation in the Lis1 defecient hepatocytes. In addition, Golgi was disorganized in Lis1 deficient livers. These mutants exhibited increased hepatocyte ploidy and accelerated development of liver cancer when treated with DEN. Taken together, these findings suggest that Lis1 is involved in the development and progression of liver diseases from steatosis to liver cancer and provide a useful model for delineating the molecular pathways that lead to these diseases.

2018-02-15 | GSE108096 | GEO

LIS1 RNA-binding orchestrates the mechanosensitive properties of embryonic stem cells in AGO2-dependent and independent ways

Project description:Lissencephaly-1 (LIS1) is associated with neurodevelopmental diseases and is known to regulate the molecular motor cytoplasmic dynein activity. Here we show that LIS1 is essential for the viability of mouse embryonic stem cells (mESCs), and it governs the physical properties of these cells. LIS1 dosage substantially affects gene expression, and we uncovered an unexpected interaction of LIS1 with RNA and RNA-binding proteins, most prominently the Argonaute complex. We demonstrate that LIS1 overexpression partially rescued the extracellular matrix (ECM) expression and mechanosensitive genes conferring stiffness to Argonaute null mESCs. Collectively, our data transforms the current perspective on the roles of LIS1 in post-transcriptional regulation underlying development and mechanosensitive processes.

2023-05-04 | GSE198390 | GEO

Transient knockdown of LIS1 results in seizures, differential gene expression and a neuronal migration disorder in developing zebrafish

Project description:Mutation or deletion of LIS1 (Lissencephaly-1) underlies classical lissencephaly, a migration disorder resulting in brain malformation, epilepsy and mental retardation. Orthologues for LIS1 genes (lis1a and lis1b) are ubiquitously expressed in developing zebrafish larvae, but the functional consequences of Lis1 knockdown are unknown. Here we used lis1-specific morpholino oligonucleotides (MOs, targeting protein translation or mRNA splicing, respectively) to transiently knockdown Lis1 expression in zebrafish. Injection of lis1 MOs resulted in morphological changes including microcephaly. At four days post-fertilization, lis1 morphants exhibited spontaneous convulsive behavior and abnormal large-amplitude electrographic discharge resembling that seen in acute and genetic zebrafish models of epilepsy. Abnormal brain development and neuronal migration defects were observed when lis1 MO injections were made into fluorescent reporter lines demarcating interneuron distribution (Dlx5a/6a:GFP) and brain structure (GBT0133:mRFP). Microarray analysis for ~44,000 Danio rerio transcripts identified 215 up-regulated and 160 down-regulated genes. Quantitative PCR and whole-mount in situ hybridization were used to validate these results for twenty and seven genes, respectively. These findings in a simple vertebrate model reproducing neuroanatomical and epileptic hallmarks of the human condition represent a novel approach to the study of childhood seizure disorders associated with a single gene mutation 4 WT samples (sample= 10 pooled larvae) and 4 Lis1Morphants slight phenotype (sample= 10 pooled larvae) were collected at 4dpf (days post fertilization). The morphants were selected based on phenotype and seizure behavior. Both groups of fish derived from same pools of eggs

2013-06-15 | E-GEOD-47952 | biostudies-arrayexpress

Transient knockdown of LIS1 results in seizures, differential gene expression and a neuronal migration disorder in developing zebrafish

2013-06-15 | GSE47952 | GEO

RIP sequencing in PANC-1 cells to map the YBX1-binding mRNA of PANC-1 cells treated with CAF-derived Evs

Project description:Perineural invasion (PNI) is a unique biological feature of pancreatic cancer and is a key cause of pancreatic cancer metastasis, recurrence and poor postoperative survival, but its mechanism is largely unclarified. Clinical sample analysis and endoscopic ultrasonographic elasticity scoring indicated that cancer-associated fibroblasts (CAFs) are closely related to the occurrence of PNI. Furthermore, CAF-derived extracellular vesicles played an extremely important role in PNI in a dorsal root ganglion (DRG) coculture model and sciatic nerve model. Next, we demonstrated that CAFs promoted PNI via extracellular vesicle transmission of PNI-associated transcript (PIAT). To explored the potential mRNA interacted with YBX1, we we performed YBX1 RNA immunoprecipitation–sequencing (RIP-seq).

2024-04-20 | GSE264220 | GEO

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