Garcinol, an acetyltransferase inhibitor, suppresses proliferation of breast cancer cell line MCF-7 promoted by 17β-estradiol.

The acetyltransferase inhibitor garcinol, a polyisoprenylated benzophenone, is extracted from the rind of the fruit of Garcinia indica, a plant found extensively in tropical regions. Anti-cancer activity has been suggested but there is no report on its action via inhibiting acetylation against cell proliferation, cell cycle progression, and apoptosis-inhibtion induced by estradiol (E2) in human breast cancer MCF-7 cells. The main purposes of this study were to investigate the effects of the acetyltransferase inhibitor garcinol on cell proliferation, cell cycle progression and apoptosis inhibition in human breast cancer MCF-7 cells treated with estrogen, and to explore the significance of changes in acetylation levels in this process.

MiR-155 promotes proliferation of human breast cancer MCF-7 cells through targeting tumor protein 53-induced nuclear protein 1.

Background: MiR-155 has emerged as an "oncomiR", which is the most significantly up-regulated miRNA in breast cancer. However, the mechanisms of miR-155 functions as an oncomiR are mainly unknown. In this study, the aims were to investigate the effects of miR-155 on cell proliferation, cell cycle, and cell apoptosis of ERalpha (+) breast cancer cells and to verify whether TP53INP1 (tumor protein 53-induced nuclear protein 1) is a target of miR-155, and tried to explore the mechanisms of miR-155 in this process.

17β-estradiol up-regulates miR-155 expression and reduces TP53INP1 expression in MCF-7 breast cancer cells.

In estrogen responsive breast cancer cells, estradiol (E2) is a key regulator of cell proliferation and survival. MiR-155 has emerged as an "oncomiR", which is the most significantly up-regulated miRNA in breast cancer. Moreover, miR-155 is higher in ERα (+) breast tumors than ERα (-), but no one has examined whether E2 regulates miR-155 expression in MCF-7 cells.

Effect of Trastuzumab on Notch-1 Signaling Pathway in Breast Cancer SK-BR3 Cells.

Objective: To investigate the effects and mechanisms of trastuzumab on Notch-1 pathway in breast cancer cells, recognizing the significance of Notch-1 signaling pathway in trastuzumab resistance.

Methods: Immunocytochemistry staining and Western blotting were employed to justify the expression of Notch-1 protein in HER2-overexpressing SK-BR3 cells and HER2-non-overexpressing breast cancer MDA-MB-231 cells. Western blotting and reverse transcription PCR (RT-PCR) were used to detect the activated Notch-1 and Notch-1 target gene HES-1 mRNA expression after SK-BR3 cells were treated with trastuzumab.

1,25-Dihydroxyvitamin D3 inhibits growth of the breast cancer cell line MCF-7 and downregulates cytochrome P4501B1 through the COX-2/PGE2 pathway.

Cytochrome P4501B1 (CYP1B1) is responsible for tumor progression in estrogen receptor-positive breast cancer due to its key role in estrogen metabolism, which is upregulated by PGE2, the main product of COX-2 that is found to be overexpressed in many breast tumors. Previous studies reported that inhibition of the COX-2/PGE2 pathway, by 1,25-dihydroxyvitamin D3 in MCF-7 breast cancer cells. The aim of this study was to investigate if the CYP1B1 protein expression shows covariation with the COX-2 and phosphorylated ERα (p-ERα) in human breast cancer.

Protective effects of trichostatin A on liver injury in septic mice.

Aim: Acetylation is emerging as a crucial post-translational modification in controlling the expression of eukaryotic genes. Histone deacetylase (HDAC) inhibitors, developed as antitumor reagents, have recently exhibited novel anti-inflammatory properties. In the present study, the influence of HDAC inhibitor on hepatic injury during sepsis was investigated.

[Effect of HSP90 function inhibited on the telomerase and P53 mutant in breast cancer cells].

Objective: To investigate the effect of heat shock protein 90 (Hsp90) function inhibited on the telomerase activity and P53 expression in human breast cancer cells, in which a specific inhibitor geldanamycin (GA) was used to inhibit Hsp90 function.

Methods: Human breast cancer cell line MDA-MB-435s was used for the study. Proliferation of MDA-MB-435s cells was measured with MTT assay.

[Effect of Janus kinase inhibitor AG490 on invasion and metastasis of human breast cancer cells].

Objective: To investigate the effect of Janus kinase (JAK) inhibitor AG490 on invasion and metastasis of the human breast cancer cell MDA-MB-231, and to explore the regulating role of JAK-STAT3 signaling pathway when the breast cancer occurs to the invasiveness and metastasis.

Methods: The human breast cancer cell MDA-MB-231 was used as the research object, and AG490 was as Janus kinase inhibitor. The adhesion of MDA-MB-231 cell attaching to matrigel was measured with MTT assay.

[Effects of a JAK inhibitor, AG490, on proliferation and survivin expression of breast cancer cell line MDA-MB-231].

Background & Objective: Many researches have proven that Survivin is expressed abundantly and is involved in tumorigenesis and prognosis of breast cancers. However, the signal transduction pathway of Survivin in breast cancer cells is still not clear. This study was to investigate the effects of AG490, a JAK enzyme inhibitor, on the expression of Survivin and on the proliferation and apoptosis of human breast cancer cell line MDA-MB-231.

[Correlation of MUC1 expression to adhesion of breast cancer cell line MDA-MB-231].

Background & Objective: Recent researches found that an abundant production of mucin protein well correlates with tumor cell metastasis. This study was to investigate inhibitory effect of benzyl-alpha-GalNAc on production of mucin 1 (MUC1), and on adhesion and invasion of breast cancer cell line MDA-MB-231.

Methods: MDA-MB-231 cells were incubated with benzyl-alpha-GalNAc, expression of MUC1 was detected by immunohistochemistry, adhesive ability of MDA-MB-231 cells to artificial basement membrane Matrigel was measured by MTT assay.