GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Han, Cailing  (2)
Material
Publisher
Person/Organisation
Language
Years
  • 1
    In: Archives of Medical Science, Termedia Sp. z.o.o.
    Abstract: Chromobox protein homolog 3 (CBX3) has been reported to regulate a variety of cellular biological functions and play an oncogenic role in various tumor. Nevertheless, the role of CBX3 remains vague in ovarian cancer. This research aimed to assess the role and potential regulatory mechanism of CBX3 in ovarian cancer. Material and methods The CBX3 expression was determined by qRT-PCR and western blotting in ovarian cancer tissues and cell lines. Cell proliferation, cycle and apoptosis were detected by using CCK-8 assay and flow cytometry. Transwell and wound healing assay were used to determine cell invasion and migration. Furthermore, the modulation of CBX3 on NCOR2 expression and p53/p21-mediated glycolysis was confirmed. Results The expression of CBX3 was significant elevated in ovarian cancer tissues and cell lines. CBX3 knockdown inhibited cell proliferation, invasion and migration, while promoted G1/S phase blockade and cell apoptosis. Mechanism analysis verified that CBX3 downregulation increased NCOR2 expression and blocked subsequent p53/p21-mediated glucose metabolism. NCOR2 silencing and p53/p21 inhibitor treatment reversed the inhibitory effects of CBX3 knockdown on ovarian cancer cellular function. Conclusions We revealed that CBX3 promoted ovarian cancer progression by promoting p53/p21-mediated glucose metabolism via inhibiting NCOR2. These results provide a theoretical basis for the diagnosis and treatment of ovarian cancer.
    Type of Medium: Online Resource
    ISSN: 1734-1922 , 1896-9151
    Language: Unknown
    Publisher: Termedia Sp. z.o.o.
    Publication Date: 2022
    detail.hit.zdb_id: 2203781-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    In: Archives of Medical Science, Termedia Sp. z.o.o.
    Abstract: Endometriosis is a reproductive disorder closely associated with hypoxia stress. Increasing evidences have implied the important roles of angiotensin II (ANG II) receptors in the pathophysiology of endometriosis. Thus, we speculated that Azilsartan (AZL), an ANG II receptor blocker, might have an effective function in controlling endometriosis. Material and methods The endometriotic animal model was established in female SD rats (6-8 weeks old, 200-220 g). Rats were divided into sham group and endometriosis (EMS) group. Rats in EMS group were anaesthetized by halothane and a mid-ventral incision was performed to expose the bowels. Human endometrial stromal cell line T-HESC was used for the in vitro assays. The T-HESC cells were cultured in DMEM-F12 mediumwith 10% fetal bovine serum (FBS, Hyclone), and 4 mM L-glutamine, 0.25% HEPES plus necessary antibiotics (Sigma-Aldrich, USA), at 37°C in a humidified atmosphere of 5% CO2. Results The results show that upregulation of ANG II type 1 (AT1) receptor was observed in the endometriotic rat models. Treatment with AZL prevented the development of endometriotic lesions and suppressed the expressions of HIF-1α and cyclooxygenase 2 (COX-2) in endometriotic rats. In vitro assays proved that hypoxia-induced proliferation, migration, and invasion of T-HESC cells were attenuated by AZL. AZL inhibited the expression levels of hypoxia-inducible factor-1α (HIF-1α), COX-2, and prostaglandin E2 (PGE2) production in hypoxia-induced T-HESC cells. Overexpression of HIF-1α blocked the effects of AZL on T-HESC cells in response to hypoxia. Conclusions AZL showed therapeutic function on endometriosis through inhibiting hypoxia-induced cell proliferation, migration, and invasion of T-HESC cells via HIF-1α/COX-2/PGE2 signaling.
    Type of Medium: Online Resource
    ISSN: 1734-1922 , 1896-9151
    Language: Unknown
    Publisher: Termedia Sp. z.o.o.
    Publication Date: 2022
    detail.hit.zdb_id: 2203781-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...