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Motivated by quantum statistical mechanics, we propose an accurate analytical solution to the problem of BoseEinstein condensation (BEC) of ideal bosons in a two-dimensional anisotropic harmonic trap. The study reveals that the number of noncondensed bosons is characterized by an analytical function, which relates to a series expansion of q-digamma functions in mathematics. The q-digamma function is a function of temperature, boson number, and anisotropic parameter. The analytical solution describes fully the experimental results of the BEC of ideal bosons in a two-dimensional anisotropic harmonic trap. We derive the analytical expressions of the critical temperature and the condensate fraction in the thermodynamic limit. The first main conclusion is that for a fixed temperature and boson number, there is a critical anisotropic parameter, which is the precise onset of BEC in this harmonically trapped two-dimensional system. The second main conclusion is that the critical temperature in a two-dimensional anisotropic harmonic trap is larger than that in a two-dimensional isotropic harmonic trap. Key words: rigorous results in statistical mechanics, Bose-Einstein condensation, cold atoms, anisotropic two-dimensional harmonic trap, q-digamma function. Motives par la mecanique statistique quantique, nous proposons une solution analytique precise du probleme du condensat de Bose-Einstein (CBE) de bosons parfaits dans un piege harmonique anisotrope 2D. L'etude revele que le nombre de bosons non condenses est caracterise par une fonction analytique qui se rattache a une expansion en serie de fonctions mathematiques q-digamma. La fonction q-digamma depend de la temperature, du nombre de bosons et du parametre d'anisotropie. La solution analytique decrit completement les resultats experimentaux du CBE de bosons parfaits dans un piege harmonique anisotrope 2D. Nous derivons alors les expressions analytiques pour la temperature critique et la fraction condensee dans la limite thermodynamique. La premiere conclusion importante est que pour une temperature et un nombre de bosons donnes, il y a un parametre critique d'anisotropie qui est precisement l'amorce du CBE dans ce systeme 2D piege harmoniquement. La deuxieme conclusion importante est que la temperature critique dans un piege harmonique anisotrope 2D est plus elevee que dans un piege equivalent isotrope. [Traduit par la Redaction] Mots-cles : resultats rigoureux en mecanique statistique, condensat de Bose-Einstein, atomes froids, piege harmonique anisotrope 2D, fonction q-digamma., 1. Introduction The boson systems in which the boson number is conserved possess a common quantum property that a macroscopically large number of bosons tend to occupy the ground state [...]

The CUE domains are small, moderately conserved ubiquitin-binding domains of ~40 amino acids; they are found in a variety of eukaryotic proteins (1,2). These proteins are involved in the recognition [...], Endocrine resistance is a major obstacle to hormonal therapy for breast cancers. Although reduced expression of estrogen receptor-α (ER-α) is a known contributing factor to endocrine resistance, the mechanism of ER-α downregulation in endocrine resistance is still not fully understood. Here we report that CUE domain-containing protein-2 (CUEDC2), a ubiquitin-binding motif-containing protein, is a key factor in endocrine resistance in breast cancer. We show that CUEDC2 modulates ER-α protein stability through the ubiquitin-proteasome pathway. Through the study of specimens from a large cohort of subjects with breast cancer, we found a strong inverse correlation between CUEDC2 and ER-α protein expression. Notably, subjects with tumors that highly expressed CUEDC2 had poor responsiveness to tamoxifen treatment and high potential for relapse. We further show that ectopic CUEDC2 expression impaired the responsiveness of breast cancer cells to tamoxifen. Therefore, our findings suggest that CUEDC2 is a crucial determinant of resistance to endocrine therapies in breast cancer.

Introduction Carcinogenesis involves sequential mutations in genes that play key roles in the control of cell growth and proliferation (1). These mutations usually lead to either the loss of tumor [...], Activating mutations in Ras proteins are present in about 30% of human cancers. Despite tremendous progress in the study of Ras oncogenes, many aspects of the molecular mechanisms underlying Ras-induced tumorigenesis remain unknown. Through proteomics analysis, we previously found that the protein Gankyrin, a known oncoprotein in hepatocellular carcinoma, was upregulated during Ras-mediated transformation, although the functional consequences of this were not clear. Here we present evidence that Gankyrin plays an essential role in Ras-initiated tumorigenesis in mouse and human cells. We found that the increased Gankyrin present following Ras activation increased the interaction between the RhoA GTPase and its GDP dissociation inhibitor RhoGDI, which resulted in inhibition of the RhoA effector kinase Rho-associated coiled coil-containing protein kinase (ROCK). Importantly, Gankyrin-mediated ROCK inhibition led to prolonged Akt activation, a critical step in activated Ras-induced transformation and tumorigenesis. In addition, we found that Gankyrin is highly expressed in human lung cancers that have Ras mutations and that increased Gankyrin expression is required for the constitutive activation of Akt and tumorigenesis in these lung cancers. Our findings suggest that Gankyrin is a key regulator of Ras-mediated activation of Akt through inhibition of the downstream RhoA/ROCK pathway and thus plays an essential role in Ras-induced tumorigenesis.

DNA damage triggers cell cycle arrest to provide a time window for DNA repair. Failure of arrest could lead to genomic instability and tumorigenesis. DNA damage-induced G1 arrest is generally achieved by the accumulation of Cyclin-dependent kinase inhibitor 1 (p21). However, p21 is degraded and does not play a role in UV-induced G1 arrest. The mechanism of UV-induced G1 arrest thus remains elusive. Here, we have identified a critical role for CUE domain-containing protein 2 (CUEDC2) in this process. CUEDC2 binds to and inhibits anaphase-promoting complex/cyclosome-Cdh1 (APC/C(Cdh1)), a critical ubiquitin ligase in G1 phase, thereby stabilizing Cyclin A and promoting G1-S transition. In response to UV irradiation, CUEDC2 undergoes ERK1/2-dependent phosphorylation and ubiquitin-dependent degradation, leading to APC/C(Cdh1)-mediated Cyclin A destruction, Cyclin-dependent kinase 2 inactivation, and G1 arrest. A nonphosphorylatable CUEDC2 mutant is resistant to UV-induced degradation. Expression of this stable mutant effectively overrides UV-induced G1-S block. These results establish CUEDC2 as an APC/C(Cdh1) inhibitor and indicate that regulated CUEDC2 degradation is critical for UV-induced G1 arrest.

Objective: To establish Gankyrin knocking down 4T1-luc cell model and detect the effects of Gankyrin expression on breast cancer metastasis., Methods: 4T1-luc cells carrying shGankyrin construct were established by lentivirus infection and antibiotic screening. Western blotting and real-time PCR were used to check the expression levels of Gankyrin. In vivo imaging system was used to monitor the effects of Gankyrin knocked down on cell growth and tumor metastasis after the in situ implantation of Gankyrin knocking down 4T1-luc cells in BALB/c mice., Results: The cell expression decreased at the protein and mRNA levels. Gankyrin mRNA expression in different shGankyrin 4T1-luc cells was respectively 4.9%, 25.1% and 69.8% versus the control cells. ShGankyrin#2 4T1-luc cells were chosen for in situ implantation into BAL/c mice because luminescent intensity was consistent with cell numbers. The photon flux of lung metastatic tumor induced by Gankyrin knocking down 4T1-luc cell was 3.02 × 10(6), while that of lung metastasis induced by control cells was 10.9 × 10(6). The differences between two groups were significant. In pathology, Gankyrin was detected positive in lung metastasis tumors induced by control group. However, Gankyrin was negative in the Gankyrin knockdown group., Conclusions: Lentivirus infection may be effectively used to establish Gankyrin knocking down 4T1-luc cell model. Because of its involvement in the in vivo pulmonary metastasis of breast cancers, Gankyrin should be a novel target for tumor therapy.