RESUMO
Prostate cancer is one of the most lethal malignancies, and androgen deprivation therapy remains the mainstay of treatment for prostate cancer patients. Although androgen deprivation can initially come to remission, the disease often develops into castration-resistant prostate cancer (CRPC), which is still dependent on androgen receptor (AR) signaling and is related to a poor prognosis. Some success against CRPC has been achieved by drugs that target AR signaling, but secondary resistance uninterrupted emerges, and new therapies are urgently needed. In this study, we identified a potent small molecule compound, ZY-444, that suppressed PCa cells proliferation and metastasis, and inhibited tumor growth both in subcutaneous. Transcriptome sequencing analysis showed that TNFAIP3 was significantly elevated in prostate cancer cells after ZY-444 treatment. Further studies through overexpression of TNFAIP3 confirmed that TNFAIP3, as a direct target gene of ZY-444, contributes to the functions of ZY-444. In addition, we demonstrated the effects of TNFAIP3 on prostate cancer cell apoptosis, migration and proliferation to elucidate the mechanism of ZY-444. We found that TNFAIP3 inhibited the TNF signaling pathway, which could inhibit cell migration and proliferation and contribute to apoptosis. Overall, these findings highlighted TNFAIP3 as a tumor suppressor gene in the regulation of the progression and metastatic potential of prostate cancer and that targeting TNFAIP3 by ZY-444 might be a promising strategy for prostate cancer treatment.
RESUMO
The structure of the title salt, (C(6)H(14)N)(2)[CuBr(4)], is built up from cyclo-hexyl-ammonium cations and tetra-bromidocuprate anions, the latter being located on an inversion center. In the crystal, anions and cations are inter-connected by N-Hâ¯Br hydrogen bonds, forming ribbons parallel to [0-11].
RESUMO
The title compound, C(7)H(14)NO(+)·Br(-), was formed by reaction of 4-allyl-morpholine and hydrogen bromide. In the crystal, mol-ecules are connected via N-Hâ¯Br and C-Hâ¯Br hydrogen bonds, forming a three-dimensional network.
RESUMO
In the title mol-ecular salt, 2C(6)H(11)NH(3) (+)·C(8)H(4)O(4) (2-), the terephthalate dianion is close to being planar (r.m.s. deviation = 0.049â Å). In the crystal, the cations and anions are linked by N-Hâ¯O hydrogen bonds into (010) sheets. Of the four terephthalate O atoms, two accept two hydrogen bonds each and two accept one hydrogen bond each.
RESUMO
In the title compound, C(12)H(9)N(4)O(+)·C(7)H(5)O(2) (-), π-π stacking inter-actions [centroid-centroid distance = 3.6275â (14) â Å] stabilize the crystal structure. The dihedral angles between the central ring and the terminal rings are 3.27â (12) and 10.30â (13)°.
RESUMO
In the title compound, C(4)H(4)N(4)O, both H atoms bonded to one methyl-ene C atom are involved in C-Hâ¯N hydrogen-bonding inter-actions; one of the inter-actions results in dimers of the title mol-ecule lying about inversion centers in R(2) (2)(12) motifs and the other forms chains of mol-ecules lying along the c axis.
RESUMO
In the crystal structure of the title compound, C(6)H(9)N(2) (+)·C(6)H(4)NO(3) (-)·C(6)H(5)NO(3), ions and mol-ecules are connected via inter-molecular N-Hâ¯O, N-Hâ¯N, O-Hâ¯O and C-Hâ¯O hydrogen bonds into a three-dimensional network.
RESUMO
In the title salt, C(8)H(14)N(2) (2+)·2Br(-), the cation has a crystallographically imposed centre of symmetry. The compound is isostructural with the chloride analogue. In the crystal structure, the cations and anions are connected via N-Hâ¯Br hydrogen bonds, forming layers parallel to the bc plane.
RESUMO
In the title compound, C(2)H(5)N(2) (+)·BF(4) (-), the cations and anions are connected via inter-molecular N-Hâ¯F and C-Hâ¯F hydrogen bonds, forming a three-dimensional network.
RESUMO
In the title compound, C(12)H(10)N(4)O(+)·2Br(-)·H(2)O, the cation is approximately planar: the terminal rings make a dihedral angle of 7.91â (6)° with each other and dihedral angles of 6.02â (1) and 6.50â (8)° with the central ring. It is linked to the bromide anions and water mol-ecules by N-Hâ¯Br hydrogen bonds. In addition, O-Hâ¯Br and N-Hâ¯Br hydrogen bonds link these units into a three-dimensional network. C-Hâ¯N, C-Hâ¯Br and N-Hâ¯O inter-actions are also observed.
RESUMO
Artemisia rupestris L. is the perennial herb of rupestris belonging to Artemisia (Compositae), which is wildly distributed in Xinjiang (China), middle Asia, and Europe. It is known to have anti-inflammatory, hepatoprotective, immune function regulation, and gastrointestinal function regulation effects. AR is used to treat digestive diseases, but the effects of AR on antifunctional dyspepsia (FD) activity have not yet been reported. In this study, we aimed to investigate the therapeutic effects of Artemisia rupestris L. extract (ARE) on gastrointestinal hormones and brain-gut peptide in functional dyspepsia (FD) rats. Sixty Sprague-Dawley rats were randomly divided into 6 groups. An FD rat model was established by irregular tail clamp stimulation for 14 days except the blank group. After FD rat models, the blank group and model group were given menstruum, and the medicated rats were given corresponding medicine for 14 days. The general observations, bodyweight, and food intake were observed, and the content of serum gastrin (GAS), plasma motilin (MTL), plasma vasoactive intestinal peptide (VIP), and plasma somatostatin (SS) by the enzyme-linked immunosorbent assay was observed. The content of plasma VIP and plasma SS in the ARE group was significantly lower than in the model group, and the content of serum GAS and plasma MTL was increased in the ARE group; the GAS expression of antrum and hypothalamus was increased in the ARE group, and SS expression of antrum and hypothalamus was decreased in the ARE group by immunohistochemical detection; the results of semiquantitative reverse transcription polymerase chain reaction (RT-PCR) indicate that ARE inhibits the mRNA expression of VIP. Our results suggest that ARE can recover gastrointestinal hormone levels and regulation of the peripheral and central nervous system and alter gut peptide levels, which confirm the therapeutic effect of ARE on functional dyspepsia.