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Expresson data from lncRNA LINC01929 knockdown in MCF7 and MDA-MB-231 breast cancer cell lines

ABSTRACT: LncRNA LINC01929 was knocked down using anti-LINC01929 antisense oligonucleotides (ASOs) in the ER+ breast cancer cell line MCF7 and the triple-negative breast cancer cell line MDA-MB-231.

ORGANISM(S): Homo sapiens

PROVIDER: GSE277314 | GEO | 2025/07/31

REPOSITORIES: GEO

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mIcroRNA sequencing of LINC01929 KD knockdown and control samples in MCF7 and MDA-MB-231 breast cancer cell lines

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Expression data from lncRNA AL078604.2 and LINC01269 knockdown in MDA-MB-231, MDA-MB-468 and SKBR3 breast cancer cell lines

Project description:Breast cancer subtype-specific lncRNAs AL078604.2 and LINC01269 were knockdown in breast cancer cell lines LncRNA AL078604.2 was knockdown by an anti-AL076804.2 antisense oligonucleotides (ASOs) in triple-negative breast cancer cell lines MDA-MB-231 and MDA-MB-468 breast cancer cells. LncRNA LINC01269 was knockdown by an anti-LINC01269 ASOs in HER2+ SKBR3 breast cancer cells. To ensure the initial presence of AL078604.2 and LINC01269 in their respective cell lines, qPCR analysis was performed to confirm their expression levels prior to knockdown experiments. The effectiveness of knockdown was confirmed by qPCR analysis, which validated the reduction in AL078604.2 and LNC01269 expression in their corresponding cell lines following ASO treatment.

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Project description:Human telomeres were one of the first discovered and characterized sequences forming quadruplex structures. Association of these structures with oncogenic and tumor suppressor proteins suggests their important role in cancer development and therapy efficacy. Since cationic porphyrin TMPyP4 is known as G-quadruplex stabilizer and telomerase inhibitor, the aim of the study was to analyze the anticancer properties of this compound in two different human breast-cancer MCF7 and MDA-MB-231 cell lines. The cytotoxicity of TMPyP4 alone or in combination with doxorubicin was measured by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromid) and clonogenic assays, and the cell-cycle alterations were analyzed by flow cytometry. Telomerase expression and activity were evaluated using qPCR and telomeric repeat amplification protocol (TRAP) assays, respectively. The contribution of G-quadruplex inhibitor to protein pathways engaged in cell survival, DNA repair, adhesion, and migration was performed using immunodetection. Scratch assay and functional assessment of migration and cell adhesion were also performed. Consequently, it was revealed that in the short term, TMPyP4 neither revealed cytotoxic effect nor sensitized MCF7 and MDA-MB-231 to doxorubicin, but altered breast-cancer cell adhesion and migration. It suggests that TMPyP4 might substantially contribute to a significant decrease in cancer cell dissemination and, consequently, cancer cell survival reduction. Importantly, this effect might not be associated with telomeres or telomerase.

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Project description:Currently the greatest challenge in oncology is the lack of homogeneity of the lesions where different cell components respond differently to treatment. There is growing consensus that monotherapies are insufficient to eradicate the disease and there is an unmet need for more potent combinatorial treatments. We have previously shown that hypericin photodynamic therapy (HYP-PDT) triggers electron transport chain (ETC) inhibition in cell mitochondria. We have also shown that tamoxifen (TAM) enhances cytotoxicity in cells with high respiration, when combined with ETC inhibitors. Herein we introduce a synergistic treatment based on TAM chemotherapy and HYP-PDT. We tested this novel combinatorial treatment (HYPERTAM) in two metabolically different breast cancer cell lines, the triple-negative MDA-MB-231 and the estrogen-receptor-positive MCF7, the former being quite sensitive to HYP-PDT while the latter very responsive to TAM treatment. In addition, we investigated the mode of death, effect of lipid peroxidation, and the effect on cell metabolism. The results were quite astounding. HYPERTAM exhibited over 90% cytotoxicity in both cell lines. This cytotoxicity was in the form of both necrosis and autophagy, while high levels of lipid peroxidation were observed in both cell lines. We, consequently, translated our research to an in vivo pilot study encompassing the MDA-MB-231 and MCF7 tumor models in NOD SCID-γ immunocompromised mice. Both treatment cohorts responded very positively to HYPERTRAM, which significantly prolonged mice survival. HYPERTAM is a potent, synergistic modality, which may lay the foundations for a novel, composite anticancer treatment, effective in diverse tumor types.

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Expresson data from lncRNA LINC01929 knockdown in MCF7 and MDA-MB-231 breast cancer cell lines

Project description:Expresson data from lncRNA LINC01929 knockdown in MCF7 and MDA-MB-231 breast cancer cell lines

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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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Expression data from parental MDA-MB-231 cells and MDA-MB-231(SA) variant

Project description:Since bone metastatic breast cancer is an incurable disease, causing significant morbidity and mortality, understanding of the underlying molecular mechanisms would be highly valuable. Here, we describe in vitro and in vivo evidence for the importance of serine biosynthesis in the metastasis of breast cancer to bone. We first characterized the bone metastatic propensity of the MDA-MB-231(SA) cell line variant as compared to the parental MDA-MB-231 cells by radiographic and histological observations in the inoculated mice. Genome-wide gene expression profiling of this isogenic cell line pair revealed that all the three genes involved in the L-serine biosynthesis pathway, phosphoglycerate dehydrogenase (PHGDH), phosphoserine aminotransferase 1 (PSAT1), and phosphoserine phosphatase (PSPH) were upregulated in the highly metastatic variant. This pathway is the primary endogenous source for L-serine in mammalian tissues. Consistently, we observed that the proliferation of MDA-MB-231(SA) cells in serine-free conditions was dependent on PSAT1 expression. In addition, we observed that L-serine is essential for the formation of bone resorbing human osteoclasts and may thus contribute to the vicious cycle of osteolytic bone metastasis. High expression of PHGDH and PSAT1 in primary breast cancer was significantly associated with decreased relapse-free and overall survival of patients and malignant phenotypic features of breast cancer. In conclusion, high expression of serine biosynthesis genes in metastatic breast cancer cells and the stimulating effect of L-serine on osteoclastogenesis and cancer cell proliferation indicate a functionally critical role for serine biosynthesis in bone metastatic breast cancer and thereby an opportunity for targeted therapeutic interventions.

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