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POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [HMLER_sublines]

ABSTRACT: We conduct transcriptome comparison of HMLER-derived CD44H,CD44LS and CD44L subpopulation cells to gain transcriptomic insights on the differences between breast cancer stem cells and non-breast cancer stem cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE130575 | GEO | 2020/03/16

REPOSITORIES: GEO

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POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [PTX3_OE]

Project description:We conduct transcriptome comparison of control and PTX3-overexpressed HMLER cells to gain genomic insights on the biological processes that PTX3 is involved in breast cancer cells.

2020-03-16 | GSE130572 | GEO

POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [MCF10AT_POSH2_OE]

Project description:We conduct transcriptome comparison of control and POSH2-overexpressed MCF10AT cells to gain genomic insights on the biological processes that POSH2 is involved in breast cancer cells.

2020-03-16 | GSE130576 | GEO

POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation

Project description:POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation

| PRJNA540666 | ENA

POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [MCF10AT_POSH2_OE]

Project description:POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [MCF10AT_POSH2_OE]

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POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [HMLER_sublines]

Project description:POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [HMLER_sublines]

| PRJNA540669 | ENA

POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [PTX3_OE]

Project description:POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [PTX3_OE]

| PRJNA540670 | ENA

SH3RF3 promotes breast cancer stem-like properties via JNK activation and PTX3 upregulation.

Project description:Cancer stem-like cells (CSCs) are the tumorigenic cell subpopulation and contribute to cancer recurrence and metastasis. However, the understanding of CSC regulatory mechanisms remains incomplete. By transcriptomic analysis, we identify a scaffold protein SH3RF3 (also named POSH2) that is upregulated in CSCs of breast cancer clinical tumors and cancer cell lines, and enhances the CSC properties of breast cancer cells. Mechanically, SH3RF3 interacts with the c-Jun N-terminal kinase (JNK) in a JNK-interacting protein (JIP)-dependent manner, leading to enhanced phosphorylation of JNK and activation of the JNK-JUN pathway. Further the JNK-JUN signaling expands CSC subpopulation by transcriptionally activating the expression of Pentraxin 3 (PTX3). The functional role of SH3RF3 in CSCs is validated with patient-derived organoid culture, and supported by clinical cohort analyses. In conclusion, our work elucidates the role and molecular mechanism of SH3RF3 in CSCs of breast cancer, and might provide opportunities for CSC-targeting therapy.

| S-EPMC7237486 | biostudies-literature

POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-03-16 | GSE130577 | GEO

Transformed Human Breast Epithelial Cell Types vs. Normal Cell-of-Origin

Project description:The gene expression of two different tumorigenic human breast epithelial cell types (HMLER and BPLER) is compared with their immortalized parental cell-of-origin (HME and BPE). Keywords: breast cancer, cell-of-origin, HMEC, BPEC,metastasis, tumor stem cells, tumor initiating cells, breast adenocarcinoma

2007-08-15 | GSE6885 | GEO

Next Generation Sequencing and differential expression analysis in stem-like vs. non-stem breast cancer cells in response to HDAC1 and HDAC7 knockdown

Project description:Purpose: We performed RNA-seq differential expression analysis after 72h HDAC1 and HDAC7 knockdown in order to evaluate the transcriptional regulation exerted by HDAC1 and HDAC7 in a stem-like (BPLER) vs. non-stem (HMLER) breast cancer (BrCa) cell model (please search for keywords "BPLER" or "HMLER" in GEO to access over 240 associated data sets). Results: HDAC7 knockdown by a pool of siRNAs resulted in altered expression of nearly three times the genes in BPLER vs. HMLER cells (2545 vs. 763), with the two cell types sharing altered expression of 328 genes. In stem-like BPLER cells, HDAC7 knockdown caused significant alterations in gene expression (1068 down and 1477 up). Fewer genes, less than half of BPLER, were altered in non-stem HMLER cells (448 down and 315 up), with 199 repressed and 129 activated genes shared between the two cell types. In contrast, 72h HDAC1 knockdown resulted in nearly equal numbers of altered genes in BPLER vs. HMLER cells (3187 vs. 2627), with the two cell types sharing altered expression of 637 genes. Moreover, the number of repressed (1570 vs. 1307) and activated (1617 vs. 1320) gene transcripts was similar in the two cell types In HMLER cells, HDAC7 knockdown resulted in alterations of significantly fewer gene transcripts compared to HDAC1 knockdown (508 vs. 2681), in both repressed (305 vs. 1362) and activated (203 vs. 1319) transcripts. Conclusions: Cumulatively, these results highlight that HDAC7 regulates nearly three times as many genes in stem-like compared to non-stem BrCa cells. In contrast, HDAC1 regulates equal number of genes in the same cell context, suggesting a predominant association of HDAC7 with the cancer stem cell phenotype.

2020-02-24 | GSE131631 | GEO

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