Tripartite motif-containing 14 (TRIM14) abnormally expressed in several human cancers. However, the function and expression of TRIM14 in human breast cancer were still largely unknown. To understand biological function of TRIM14 in breast cancer, we measured expression level of TRIM14. Cell proliferation and cell apoptosis were measured after TRIM14 overexpression or knockdown. The upregulation of TRIM14 was found in human breast cancer specimens and cell lines. Deduction of TRIM14 inhibited cell proliferation but increased cell apoptosis in BT474 and MDA-MB-231 cell lines. Further study showed that knockdown of TRIM14 up-regulated the expression of BAX, while down-regulated the expression of BCL2. Meanwhile the expression of SHP-1 was increased and the phosphorylation of STAT3 (p-STAT3) was inhibited. Conversely, overexpression of TRIM14 had the opposite effects. Additional, Cryptotanshinone, a STAT3 inhibitor, inhibited cell proliferation but increased cell apoptosis in BT474 and MDA-MB-231 cell lines. In conclusion, TRIM14 may act as oncogene in human breast cancer and may be a novel strategy for human breast cancer.
Breast cancer is a highly prevalent disease affecting women. The association of IQ motif containing GTPase-activating protein 3 (IQGAP3) and breast cancer is poorly defined. Here we reported that IQGAP3 is a key regulator of cell proliferation and metastasis during breast cancer progression. The expression of IQGAP3 was significantly increased in breast tissues compared to nontumor tissues at both protein and mRNA levels. Furthermore, IQGAP3 had a high expression level in ZR-75-30 and BT474 compared to other breast cancer cell lines. Depletion of IQGAP3 through RNA interference in ZR-75-30 and BT474 significantly inhibited cell proliferation. More importantly, IQGAP3 silencing in breast cancer cells notably repressed cell migration and invasion. Further analysis suggested that inhibition of cell proliferation and metastasis was associated with some proteins, including p53, MMP9, Snail, CDC42, p-ERK1/2, KIF2C, KIF4A, PCNA, and Twist. Since expression of IQGAP3 seems to be associated with the pathogenesis of breast cancer and suppression of it can inhibit cancer cell growth and metastasis, IQGAP3 may be a potential therapeutic target in human breast cancer.
BackgroundBreast cancer (BC), a prevalent and heterogeneous disease of glandular breast tissue, is the most common cancer in women. The interaction between Kaempferol and IQ motif containing GTPase-activating protein 3 (IQGAP3) in BC and its underlying mechanism are poorly defined.Material/MethodsAfter natural phytochemicals treatment, the expression of IQGAP3 in BC cells (ZR-75-30 and BT474) was detected by real-time PCR. Then, the proliferation and apoptosis in BC cells with different gradient concentrations (10, 25, 50, and 100 μmol/l) of Kaempferol treatment were detected. After treatment with Kaempferol or epidermal growth factor (EGF), we assessed apoptosis and expression of related genes.ResultsWe found that natural phytochemicals, especially Kaempferol, decreased IQGAP3 expression in BC cells. Kaempferol significantly induced proliferation inhibition and apoptosis in BC cells, concurrent with decreased IQGAP3 expression. Upregulation of IQGAP3 inhibited apoptosis in BC cells, along with increased expression of phosphorylated extracellular signal-regulated kinases 1/2 (p-ERK1/2) and B cell lymphoma 2 (Bcl2) and decreased Bcl-2-associated X protein (Bax) expression, which was counteracted by Kaempferol treatment. EGF markedly inhibited Kaempferol-induced apoptosis in BC cells, and ERK1/2 inhibitor PD98059 had an effect similar to that of Kaempferol.ConclusionsIQGAP3 may be a potential target gene for Kaempferol in the treatment of BC, and upregulation of IQGAP3 inhibits Kaempferol-induced apoptosis in BC cells by ERK1/2 signaling activation. Targeting IQGAP3 may contribute to the study of natural phytochemicals as anti-tumor drugs in BC.
Background: Currently, more and more circular RNAs (circRNAs) have been identified to exert their functions in tumor progression, including colorectal cancer (CRC). However, the role of circSEC24A (circ_0003528) in CRC remains unknown.Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the levels of circSEC24A, SEC24A and microRNA-488-3p (miR-488-3p). The characterization of circSEC24A was investigated by Actinomycin D and RNase R digestion assays. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay was used to assess cell proliferation. Flow cytometry analysis was adopted for cell apoptosis and cell cycle process. Transwell assay was employed to evaluate cell migration and invasion. Western blot assay was performed to determine protein levels. Dual-luciferase reporter assay was utilized to explore the relationship between miR-488-3p and circSEC24A or transmembrane protein 106B (TMEM106B). Murine xenograft model was constructed to explore the effect of circSEC24A in vivo .Results: CircSEC24A level was increased in CRC tissues and cells. CircSEC24A deficiency impeded cell proliferation, cell cycle process, migration and invasion and induced apoptosis in CRC cells in vitro and blocked tumorigenesis in vivo . MiR-488-3p was a target of circSEC24A and miR-488-3p was downregulated in CRC tissues and cells. The inhibitory effect of circSEC24A silencing on CRC cell progression was restored by miR-488-3p inhibition. Moreover, TMEM106B could be negatively regulated by miR-488-3p via acting as a downstream gene of miR-488-3p. MiR-488-3p overexpression decelerated CRC cell progression by targeting TMEM106B.Conclusion: CircSEC24A facilitated CRC progression by regulating miR-488-3p/TMEM106B axis, which might provide a promising treatment approach for CRC.
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