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

ABSTRACT: 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).

ORGANISM(S): Homo sapiens

PROVIDER: GSE264220 | GEO | 2024/04/20

REPOSITORIES: GEO

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mRNA profile of PANC-1 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 determine how CAF EVs exert its function, we performed mRNA sequencing on PANC-1 treated with CAFs-derived EVs

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lncRNA profile of PANC-1 treated with CAFs 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. To explore the lncRNA packaged in CAFs EVs transmitted to PANC-1, we conducted the lncRNA profile of PAN-1 treated with CAFs derived EVs.

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lncRNA profile of CAFs 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. To explore the lncRNA packaged in CAFs EVs, we conducted the lncRNA profile of CAFs derived EVs.

2024-04-29 | GSE265764 | GEO

lncRNA profile of CAFs isolated from Pancreatic cancer

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. To explore the lncRNA packaged in CAFs EVs, we conducted the lncRNA profile of CAFs isolated from pancreatic cancer

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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

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.

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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

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Endosomal trafficking bypassed by RAB5B-CD109 interplay promotes axonogenesis in KRAS-mutant pancreatic cancer

Project description:Perineural invasion (PNI) represents a unique biological feature causing the poor prognosis of pancreatic ductal adenocarcinoma (PDAC), especially with KRAS mutation. Extracellular vesicle (EVs)-packaged circRNAs function as essential mediator for tumor microenviroment communication to trigger PDAC cells invading into the surrounding regions and lead to distant metastasis. However, the regulatory mechanism of exosomal circRNA in PNI of KRAS-mutated PDAC has not been elucidated. Herein, we identified an KRASG12D-mutation responsive exosomal circRNA-circPNIT, which was positively correlated with PNI of PDAC. Functionally, KRASG12D PDAC-derived EV-packaged circPNIT promotes axonogenesis and PNI both in vitro and in vivo. Mechanistically, circPNIT-mediated Rab5B-CD109 interplay bypassed traditional endosomal trafficking to anchor Rab5B in the lipid rafts of multivescular body and fostered the secretion of circPNIT as a cargo of CD109+EVs. Subsequently, CD109+EVs achieved the targeted delivery of circPNIT to neurons by recognizing their surface receptor TRPV1 and facilitated DSCAML1 transcription-induced axonogenesis, which in turn enhanced the PNI by activating GFRα1/RET pathway. Importantly, we established an engineered si-cirPNIT-loaded CD109+EVs to dramatically inhibit PNI of PDAC in a KRASG12D/+ Trp53R172H/+ Pdx-1-Cre mice model. Collectively, Our findings highlight the mechanism underlying EV-packaed circRNA mediating PNI of KRAS mutated-PDAC dependent of a Rab5B endosomal bypass, supporting circPINT as an effective target for the treatment of neuro-metastatic PDAC

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

Project description: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.

2025-01-01 | GSE282822 | GEO

CD9, a key mediator of pancreatic cancer cell aggressiveness driven by CAFs-derived extracellular vesicles

Project description:While of growing interest in pancreatic cancer (PC) field, the stromal-tumor cells crosstalk lags behind in terms of biomarkers and therapeutic options improving the clinical armamentarium. Knowledge on cellular communications was drastically enhanced following the discovery of extracellular vesicles (EVs), a powerful process of intercellular exchanges. We previously described a new stromal-tumor cell crosstalk mediated by Cancer-Associated Fibroblasts (CAFs)-derived ANXA6+-EVs, supporting pancreatic cancer cell aggressiveness in hostile areas of PC. In this study, using mass spectrometry analyses to investigate CAFs-derived EVs' cargo, we report that CD9 is a key member of the ANXA6/LRP1/TSP1 complex present in PC-associated CAFs-derived ANXA6+-EVs. We determined that CD9 is expressed by PC-associated CAFs in vivo as well as in vitro following physiopathologic culture conditions. Targeting CD9 impaired CAFs-derived ANXA6+-EVs uptake by pancreatic cancer cells, which consequently decreases their migratory abilities. Signaling pathway arrays highlighted p38/MAPK as activated in pancreatic cancer cells following CAFs-derived ANXA6+/CD9+-EVs uptake. The use of CD9 blocking antibody, p38 siRNA or chemical inhibitors impaired pancreatic cancer cells abilities following incubation with CAFs-derived ANXA6+/CD9+-EVs. Finally, we revealed CD9 expression as an independent poor-prognosis marker in human PC samples. Collectively our data highlight the key role of CD9 in CAFs-derived ANXA6+-EVs internalization by pancreatic cancer cells and the consequent, and mandatory, activation of p38/MAPK pathway to foster their migratory abilities. Measuring the oncogenic CAFs-derived ANXA6+/CD9+-EVs then limiting their action on pancreatic cancer cells abilities might be a promising option for PC stratification and treatment.

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