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Next Generation Sequencing Facilitates Quantitative Analysis for H3K27ac mediated chromatin conformation capture of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line

ABSTRACT: CRISPRi targeting PVT1 specifically decrease PVT1-MYC interaction

ORGANISM(S): Homo sapiens

PROVIDER: GSE97585 | GEO | 2018/05/31

REPOSITORIES: GEO

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Next Generation Sequencing Facilitates Quantitative Analysis for Chromatin Immunoprecipitation of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line

Project description:CRISPRi targeting PVT1 specifically increased H3K9me3 at PVT1

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line

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Next Generation Sequencing for Chromatin accessbility by ATAC-seq for MDA-MB-231, MCF7 or HCT116 cell line

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Next Generation Sequencing Facilitates Quantitative Analysis of chromatin conformational interaction between MYC and PVT1 in MDA-MB-231, MCF7, HCT116 cancer cell line

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ChIP-seq of KLF2 Binding Site 1-targeting CRISPRi in MDA-MB-231 cells

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Next Generation Sequencing Facilitates Quantitative Analysis of PVT1 mutant alleles have distinct growth advantage which was introduced by CRISPR in MDA-MB-231 human breast cancer cell line

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Project description:Next Generation Sequencing Facilitates Quantitative Analysis of PVT1 overexpressed MDA-MB-231 cells.

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Effects of FSTL1 on cell proliferation in breast cancer cell line MDA‑MB‑231 and its brain metastatic variant MDA‑MB‑231‑BR.

Project description:In the past decades, altered Follistatin‑like 1 (FSTL1) expression has been documented in a variety of cancers, while its functional roles are poorly understood. Particularly in breast cancer, the expression of FSTL1 and its signaling pathway remain to be determined. In the present study, an elevated FSTL1 expression and a supressed cell proliferation were detected in a specific brain metastatic cell line MDA‑MB‑231‑BR (231‑BR), compared with its parental cell line MDA‑MB‑231. However, this protein was hardly detected in the other three breast cancer cell lines. Next, lentiviral vectors encoding FSTL1 or FSTL1 specific shRNAs were used to overexpress or knock down FSTL1 in MDA‑MB‑231 or 231‑BR, respectively (MDA‑MB‑231FSTL1 or 231‑BRsh FSTL1). Results showed that overexpression of FSTL1 inhibited MDA‑MB‑231 cell proliferation, while knockdown of FSTL1 in 231‑BR cells promotes cell proliferation, compared with their corresponding control groups. These results were further confirmed in nude mouse xenografts. The tumor volume in 231‑BR cell-bearing mice was significantly smaller than that of MDA‑MB‑231 group, and reduction of tumor volume was detected in MDA‑MB‑231FSTL1 cell-bearing mice compared with the control group. Previous studies revealed that TGF‑β-Smad2/3 signaling pathway was activated in 231‑BR and MDA‑MB‑231FSTL1 cells, which may contribute to the inhibited cell proliferation. In addition, Smad3 knockdown could restore the inhibition of cell proliferation induced by FSTL1 overexpression in MDA‑MB‑231FSTL1 cells, indicating that the anti‑proliferative effect of FSTL1 overexpression may be associated with Smad3 involved TGF‑β signaling pathway regulation. This study identified FSTL1 as an inhibitor of cell proliferation in MDA‑MB‑231 and 231‑BR cell lines, which may provide new insights into the development and management of breast cancer.

| S-EPMC5780039 | biostudies-literature

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