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Comparative Gene Profiling Study Between Pak1 Deficient Mouse and Human Breast Cancer Cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE72206 | GEO | 2016/07/23

SECONDARY ACCESSION(S): PRJNA293349

REPOSITORIES: GEO

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Comparative Gene Profiling Study Between Pak1 Deficient Mouse and Human Breast Cancer Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-23 | E-GEOD-72206 | biostudies-arrayexpress

Comparative gene profiling study: Pak1 deficient mouse breast cancer cells vs Pak1 wt breast cancer cells

2016-07-23 | GSE71282 | GEO

Comparative gene profiling study: Pak1 deficient mouse breast cancer cells vs Pak1 wt breast cancer cells

Project description:To identify differentially regulated genes between wild-type and Pak1 deficient mouse breast cancer cells, we performed a comparative gene profiling study by using mouse whole genome arrays. We compared the gene expression profiles of Her2 positive : Pak1 deficient cells vs Her2 positive : Pak1 wild type cells. All the experiments were performed in duplicate using tumor derived cells from two different tumors per group.

2016-07-23 | E-GEOD-71282 | biostudies-arrayexpress

Comparative gene profiling study: Pak1 deficient human breast cancer cells vs Pak1 wt breast cancer cells

2016-07-23 | GSE71283 | GEO

Comparative Gene Profiling Study Between Pak1 Deficient Mouse and Human Breast Cancer Cells

Project description:Comparative Gene Profiling Study Between Pak1 Deficient Mouse and Human Breast Cancer Cells

| PRJNA293349 | ENA

Comparative gene profiling study: Pak1 deficient human breast cancer cells vs Pak1 wt breast cancer cells

Project description:To identify differentially regulated genes between wild-type and Pak1 deficient human breast cancer cells, we performed a comparative gene profiling study by using human whole genome arrays. We compared the gene expression profiles of MCF10A.B2 cells (MCF10A cells expressing a chemically activatable form of Her2) stably expressing a Tet inducible shRNA directed against Pak1 gene. All the experiments were performed in duplicate using tumor derived cells from two different tumors per group.

2016-07-23 | E-GEOD-71283 | biostudies-arrayexpress

Phospho-antibody microarray analyses for wild-type and Pak1-deficient breast cancer cells

Project description:To identify differentially phosphorylated proteins between wild-type and Pak1-deficient mouse breast cancer cells, we performed a comparative study by using phospho-antibody arrays.

2021-12-24 | GSE192492 | GEO

Pak1, adjuvant tamoxifen therapy, and breast cancer recurrence risk in a Danish population-based study.

Project description:Background Adjuvant tamoxifen therapy approximately halves the risk of estrogen receptor-positive (ER+) breast cancer recurrence, but many women do not respond to therapy. Observational studies nested in clinical trial populations suggest that overexpression or nuclear localization of p21-activated kinase 1 (Pak1) in primary tumors predicts tamoxifen failure. Material and methods We measured the association between Pak1 expression and breast cancer recurrence in a Danish population-based case-control study. Pak1 cytoplasmic expression level and nuclear positivity were determined by immunohistochemical staining of primary breast tumors from recurrence cases and matched controls from two breast cancer populations; women diagnosed with ER-positive tumors who received at least one year of tamoxifen therapy (ER+/TAM+), and women diagnosed with ER-negative tumors who survived for at least one year (ER-/TAM-). Pak1 staining was assessed by a single, blinded pathologist, and associations were estimated with conditional logistic regression models. Results We included 541 recurrence cases and 1:1 matched controls from the ER+/TAM + group and 300 recurrence cases and 1:1 matched controls from the ER-/TAM - group. Pak1 cytoplasmic intensity was not associated with breast cancer recurrence in either group (ER+/TAM + ORadj for strong vs. no cytoplasmic staining = 0.91, 95% CI 0.57, 1.5; ER-/TAM - ORadj for strong vs. no cytoplasmic staining = 0.74, 95% CI 0.39, 1.4). Associations between Pak1 nuclear positivity and breast cancer recurrence were similarly near null in both groups. Conclusion Pak1 positivity in primary breast tumors was neither predictive nor prognostic in this prospective, population-based study.

| S-EPMC4943575 | biostudies-literature

MicroRNA-494 inhibits breast cancer progression by directly targeting PAK1.

Project description:MicroRNA (miRNA) is involved in the progression and metastasis of diverse human cancers, including breast cancer, as strong evidence has been found that miRNAs can act as oncogenes or tumor suppressor genes. Here, we show that miR-494 is decreased in human breast cancer specimens and breast cancer cell lines. Ectopic expression of miR-494 in basal-like breast cancer cell lines MDA-MB-231-LUC-D2H3LN and BT-549 inhibits clonogenic ability and metastasis-relevant traits in vitro. Moreover, ectopic expression of miR-494 suppresses neoplasm initiation as well as pulmonary metastasis in vivo. Further studies have identified PAK1, as a direct target gene of miR-494, contributes to the functions of miR-494. Remarkably, the expression of PAK1 is inversely correlated with the level of miR-494 in human breast cancer samples. Furthermore, re-expression of PAK1 partially reverses miR-494-mediated proliferative and clonogenic inhibition as well as migration and invasion suppression in breast cancer cells. Taken together, these findings highlight an important role for miR-494 in the regulation of progression and metastatic potential of breast cancer and suggest a potential application of miR-494 in breast cancer treatment.

| S-EPMC5386359 | biostudies-literature

Ki67 assessment in invasive luminal breast cancer: a comparative study between different scoring methods.

Project description:BackgroundKi67 reflects the proliferation activity in breast cancer (BC). However, an optimal method for its assessment in clinical settings has yet to be robustly defined. In this study we compared several methods to score Ki67 to identify a reliable and reproducible method for routine practice.MethodsSections from luminal BC cohort (n = 1662) were immunohistochemically stained with Ki67 and were assessed for the percentage, pattern, and intensity of expression. Ki67 positivity was evaluated using three methods: (i) quantification of Ki67-positive cells among 1000 invasive tumour cells within hotspot, (ii) average estimation of Ki67 within a defined hotspot, and (iii) average estimation of Ki67 positivity within the whole section. Time required for scoring, interobserver agreement and association with outcome were determined.ResultsThe mean percentage of Ki67 expression per 1000 cells method was 16%, while the mean value of Ki67 scores using the average estimation within hotspot and whole slide were 14% and 12%, respectively. Quantification of Ki67-positive cells within 1000 cells had the highest degree of consistency between observers, and the highest hazard ratio predicting patient outcome when compared to using different common Ki67 cutoffs, which was independent of the other two methods. Granular pattern of Ki67 expression was associated with poorer outcome as compared to the other patterns.ConclusionAssessment of Ki67 expression using quantification positive cells among 1000 tumour cells is an optimal method to achieve high reliability and reproducibility. Comment on the predominant Ki67 expression pattern would add prognostic and predictive value in luminal BC.

| S-EPMC9826086 | biostudies-literature

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