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MUC1-C Drives Lineage Plasticity in Progression to Neuroendocrine Prostate Cancer

ABSTRACT: MUC1-C Drives Lineage Plasticity in Progression to Neuroendocrine Prostate Cancer

PROVIDER: PRJNA579338 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10341413.fastq.gz	Fastqsanger.gz
	SRR10341414.fastq.gz	Fastqsanger.gz
	SRR10341415.fastq.gz	Fastqsanger.gz
	SRR10341416.fastq.gz	Fastqsanger.gz
	SRR10341417.fastq.gz	Fastqsanger.gz

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MUC1-C Drives Lineage Plasticity in Progression to Neuroendocrine Prostate Cancer

Project description:Neuroendocrine prostate cancer (NEPC) is a highly aggressive malignancy of increasing prevalence with an unmet need for targeted therapeutic approaches. The oncogenic MUC1-C protein is overexpressed in castration-resistant prostate cancer (CRPC) and NEPC; however, there is no known role for MUC1-C in driving lineage plasticity to these advanced PC phenotypes. The present studies demonstrate that upregulation of MUC1-C in androgen-independent (AI) PC cells suppresses androgen receptor (AR) axis signaling and induces the neural BRN2 transcription factor by a previously unrecognized MYC-mediated mechanism. MUC1-C activates the BRN2 pathway in association with induction of MYCN, EZH2 and NE differentiation markers (ASCL1, AURKA and SYP), which are linked to NEPC progression. We also show that MUC1-C suppresses the p53 pathway, induces the Yamanaka pluripotency factors (OCT4, SOX2, KLF4 and MYC) and drives stemness. Of potential clinical relevance, targeting MUC1-C decreases PC self-renewal capacity and tumorigenicity, supporting the treatment of CRPC and NEPC with agents directed against this oncoprotein. These findings and the demonstration that MUC1-C is upregulated and associated with suppression of AR signaling, and increases in BRN2 expression and the NEPC score in PC tissues highlight the unanticipated importance of MUC1-C as a master effector of lineage plasticity in progression to advanced PC with NE features.

2019-12-02 | GSE139335 | GEO

MUC1-C DICTATES NEUROENDOCRINE LINEAGE SPECIFICATION IN PANCREATIC DUCTAL ADENOCARCINOMAS

Project description:MUC1-C drives neuroendocrine lineage plasticity in pancreatic adenocarcinomas

2021-08-13 | GSE181961 | GEO

MUC1-C regulates lineage plasticity driving progression to neuroendocrine prostate cancer.

Project description: Not available

| S-EPMC6969104 | biostudies-literature

DNMT3B drives neuroendocrine lineage plasticity and aggressive progression in prostate cancer

Project description:DNMT3B drives neuroendocrine lineage plasticity and aggressive progression in prostate cancer

| PRJNA1292727 | ENA

MUC1 triggers lineage plasticity of Her2 positive mammary tumor

Project description:The aberrant overexpression of mucin 1 (MUC1) and human epidermal growth factor receptor 2 (HER2) are often observed in breast cancer. However, the role of concomitant of MUC1/HERR2 in the development of breast cancer has not been fully illustrated. Following analysis public microarray datasets that revealed a correlation of double positive of MUC1 and HER2 to a worse clinical outcome, we generated a mouse model overexpressing both Her2 and MUC1 cytoplasmic domain (MUC1-CD) to investigate their interaction in mammary carcinogenesis. Coexpression of Her2 and MUC1-CD confers growth advantage and promotes the development of spontaneous mammary tumors. Genomic analysis uncovers that enforced expression of MUC1-CD and Her2 induces mammary tumor lineage plasticity which is supported by gene reprogramming and mammary stem cell enrichment. With gain- and loss-of function strategies, we show that coexpression of Her2 and MUC1-CD was associated with down-regulation of TCA cycle genes in tumors. Importantly, the reduction of TCA cycle genes induced by MUC1-CD is is significantly connected to the poor prognosis in HER2+ breast cancer patients. In addition, MUC1 augments Her2 signaling pathway by inducing Her2/Egfr dimerization. These findings collectively demonstrate the vital role of MUC1-CD/Her2 collaboration in shaping mammary tumor landscape and highlight the prognostic and therapeutic implication of MUC1 in patients with Her2+ breast cancer.

2022-03-10 | GSE198239 | GEO

MUC1-C DICTATES NEUROENDOCRINE LINEAGE SPECIFICATION IN PANCREATIC DUCTAL ADENOCARCINOMAS

Project description:MUC1-C DICTATES NEUROENDOCRINE LINEAGE SPECIFICATION IN PANCREATIC DUCTAL ADENOCARCINOMAS

| PRJNA754087 | ENA

MUC1 triggers lineage plasticity of Her2 positive mammary tumor

Project description:MUC1 triggers lineage plasticity of Her2 positive mammary tumor

| PRJNA814266 | ENA

DNMT3B drives neuroendocrine lineage plasticity and aggressive progression in prostate cancer

Project description:Neuroendocrine prostate cancer (NEPC) is an aggressive, treatment-resistant subtype of prostate cancer characterized by poor prognosis and limited therapeutic options. In this study, we identify de novo DNA methyltransferase 3B (DNMT3B) as a critical driver of NEPC growth and neuroendocrine differentiation. We demonstrate that DNMT3B expression is significantly upregulated during prostate cancer progression and is essential for NEPC cell proliferation, as its genetic inhibition via CRISPR-Cas9 and inducible shRNA systems impairs tumor growth and promotes apoptosis both in vitro and in vivo. Transcriptomic profiling reveals that DNMT3B loss disrupts cell cycle regulation and suppresses neuroendocrine lineage programs by downregulating key transcription factors such as FOXA2, NEUROD1, SOX2, and INSM1. Moreover, DNMT3B is required for both the initiation and maintenance of NEPC in a human genetically engineered prostate cancer model. Pharmacological inhibition of DNMT3B with Nanaomycin A selectively suppresses NEPC tumor growth and attenuates neuroendocrine marker expression without causing systemic toxicity. These findings establish DNMT3B as a central regulator of NEPC and support its potential as a therapeutic target for this lethal cancer subtype

2026-07-30 | GSE302864 | GEO

Role of Specialized Composition of SWI/SNF Complexes in Prostate Cancer Lineage Plasticity

Project description:Advanced prostate cancer initially responds to hormonal treatment, but ultimately becomes resistant and requires more potent therapies. One mechanism of resistance seen in 10% of these patients is through lineage plasticity, which manifests in a partial or complete small cell or neuroendocrine prostate cancer (NEPC) phenotype. Here, we investigate the role of the mammalian SWI/SNF chromatin remodeling complex in NEPC. Using large patient datasets, patient-derived organoids and cancer cell lines, we identify SWI/SNF subunits that are deregulated in NEPC, demonstrate that SMARCA4 (BRG1) overexpression is associated with aggressive disease and that SMARCA4 depletion impairs prostate cancer cell growth. We also show that SWI/SNF complexes interact with different lineage-specific factors in prostate adenocarcinoma and in NEPC cells, and that induction of lineage plasticity through depletion of REST is accompanied by changes in SWI/SNF genome occupancy. These data suggest a specific role for mSWI/SNF complexes in therapy-related lineage plasticity, which may be relevant for other solid tumors.

2020-11-04 | PXD016861 | Pride

A MYC Family Switch: L-MYC Drives and Maintains Neuroendocrine Lineage Programs in Prostate Cancer

Project description:Neuroendocrine prostate cancer (NEPC) is an aggressive and therapy-resistant subtype that emerges through lineage plasticity following inhibition of the androgen receptor (AR) signaling pathway. In this study, MYCL was overexpressed in prostate adenocarcinoma C4-2B cells and knocked down in neuroendocrine prostate cancer NCI-H660 cells to investigate its role in lineage regulation. RNA-sequencing analysis revealed that MYCL overexpression suppresses AR signaling and MYC target signaling while inducing neuroendocrine-like transcriptional reprogramming. In contrast, MYCL knockdown disrupts neuroendocrine lineage identity and restores adenocarcinoma-associated gene expression programs, including reactivation of MYC. These findings suggest that MYCL plays a key role in regulating lineage plasticity and maintaining neuroendocrine transcriptional programs in prostate cancer.

2026-05-12 | GSE324984 | GEO

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