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Search results for: BMYB MYBL2

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#28902363   2017/09/05 To Up

Ginkgetin induces G2-phase arrest in HCT116 colon cancer cells through the modulation of b‑Myb and miRNA34a expression.

Ginkgetin has been reported to display antitumor activity. However, the relevant pathway integrating cell cycle regulation and signaling pathways involved in growth inhibition in CRC cells remains to be identified. In this study, ginkgetin-treated HCT116 CRC cells exhibited significant dose-dependent growth inhibition with a GI50 value of 4.0 µM for 48-h treatment, together with apoptosis, via G2-phase cell cycle arrest. When HCT116 cells were treated with 10 µM ginkgetin for 48 h, the percentage of cells in G2/M phase increased by 2.2-fold (43.25%) versus the untreated control (19.69%). Ginkgetin regulated the expression of genes that are critically involved in G2 phase arrest cells, such as b‑Myb, CDC2 and cyclin B1. Furthermore, we found that the suppression of b‑Myb expression by ginkgetin was rescued ~5.1-fold by treatment with a miR-34a inhibitor (500 nM) and b‑Myb was downregulated by >80% by 100 nM miR‑34a mimic. These data suggest that the miRNA34a/b‑Myb/cyclin B1 cascade plays a critical role in ginkgetin-induced G2 cell cycle arrest, as well as in the inhibition of HCT116 cell proliferation. Moreover, the administration of ginkgetin (10 mg/kg) reduced tumor volumes by 36.5% and tumor weight by 37.6% in the mice xenografted with HCT116 cells relative to their vehicle-treated counterparts. Therefore, ginkgetin is the first compound shown to regulate b‑Myb by modulating miR-34a, and we suggest the use of ginkgetin as an inducer of G2 arrest for the treatment of CRC.
Yu-Jin Lee, Yeong-Rim Kang, So Young Lee, Yena Jin, Dong Cho Han, Byoung-Mog Kwon

2295 related Products with: Ginkgetin induces G2-phase arrest in HCT116 colon cancer cells through the modulation of b‑Myb and miRNA34a expression.

10 ug

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#27094710   2016/05/20 To Up

Linkage of E2F1 transcriptional network and cell proliferation with respiratory chain activity in breast cancer cells.

Mitochondria are multifunctional organelles; they have been implicated in various aspects of tumorigenesis. In this study, we investigated a novel role of the basal electron transport chain (ETC) activity in cell proliferation by inhibiting mitochondrial replication and transcription (mtR/T) using pharmacological and genetic interventions, which depleted mitochondrial DNA/RNA, thereby inducing ETC deficiency. Interestingly, mtR/T inhibition did not decrease ATP levels despite deficiency in ETC activity in different cell types, including MDA-MB-231 breast cancer cells, but it severely impeded cell cycle progression, specifically progression during G2 and/or M phases in the cancer cells. Under these conditions, the expression of a group of cell cycle regulators was downregulated without affecting the growth signaling pathway. Further analysis suggested that the transcriptional network organized by E2F1 was significantly affected because of the downregulation of E2F1 in response to ETC deficiency, which eventually resulted in the suppression of cell proliferation. Thus, in this study, the E2F1-mediated ETC-dependent mechanism has emerged as the regulatory mechanism of cell cycle progression. In addition to E2F1, FOXM1 and BMYB were also downregulated, which contributed specifically to the defects in G2 and/or M phase progression. Thus, ETC-deficient cancer cells lost their growing ability, including their tumorigenic potential in vivo. ETC deficiency abolished the production of reactive oxygen species (ROS) from the mitochondria and a mitochondria-targeted antioxidant mimicked the deficiency, thereby suggesting that ETC activity signaled through ROS production. In conclusion, this novel coupling between ETC activity and cell cycle progression may be an important mechanism for coordinating cell proliferation and metabolism.
Kazunori Mori, Tetsu Uchida, Motonori Fukumura, Shigetoshi Tamiya, Masato Higurashi, Hirosato Sakai, Fumihiro Ishikawa, Motoko Shibanuma

1012 related Products with: Linkage of E2F1 transcriptional network and cell proliferation with respiratory chain activity in breast cancer cells.

50 ug1x10e7 cells10 rxns

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#24166507   2013/10/28 To Up

Human papillomavirus type 16 E7 perturbs DREAM to promote cellular proliferation and mitotic gene expression.

The study of the small DNA tumor viruses continues to provide valuable new insights into oncogenesis and fundamental biological processes. Although much has already been revealed about how the human papillomaviruses (HPVs) can transform cells and contribute to cervical and oropharyngeal cancer, there clearly is much more to learn. In this issue of Oncogene, Pang et al., doi:10.1038/onc.2013.426, demonstrate that the high-risk HPV16 E7 oncogene can promote cellular proliferation by interacting with the DREAM (DP, RB-like, E2F and MuvB) complex at two distinct phases of the cell cycle. Consistent with earlier work, HPV16 E7 can bind to the retinoblastoma tumor suppressor (RB) family member p130 (RBL2) protein and promote its proteasome-mediated destruction thereby disrupting the DREAM complex and can prevent exit from the cell cycle into quiescence. In addition, they demonstrate that HPV16 E7 can bind to MuvB core complex in association with BMYB and FOXM1 and activate gene expression during the G2 and M phase of the cell cycle. Thus, HPV16 E7 acts to prevent exit from the cell cycle entry and promotes mitotic proliferation and may account for the high levels of FOXM1 often observed in poor-risk cervical cancers.
J A DeCaprio

1406 related Products with: Human papillomavirus type 16 E7 perturbs DREAM to promote cellular proliferation and mitotic gene expression.

0.5 mg0.5 mg0.5 mg96T100 reactionsOne 96-Well Strip Micropl

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#8812502   // To Up

Mybl2 (Bmyb) maps to mouse chromosome 2 and human chromosome 20q 13.1.

Mybl2 encodes a transcription factor that is thought to play an important role in cell cycle progression. Here we report the chromosomal localization of Mybl2 in mouse and human. Using mouse Mybl2 cDNA clones as probes, we assigned Mybl2 in an interspecific backcross panel to distal Chromosome 2. Using human cDNA probes in combination with FISH analysis, we localized MYBL2 to chromosome 20q13.1, a region that is commonly deleted in myeloid disorders. Both chromosomal regions are highly homologous, and the map positions, therefore, confirm each other. However, our findings are in contrast to a previous report by Barletta et al. (Cancer Res. 51:3821-3824, 1991) that placed the MYBL2 gene on human chromosome Xq13.
K Noben-Trauth, N G Copeland, D J Gilbert, N A Jenkins, G Sonoda, J R Testa, K H Klempnauer

1500 related Products with: Mybl2 (Bmyb) maps to mouse chromosome 2 and human chromosome 20q 13.1.

100ug Lyophilized100ug Lyophilized25ml 100ug LyophilizedOne 96-Well Strip Micropl100ug Lyophilized200ug100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

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