5 results on '"Hu, Lian"'
Search Results
2. [Association of receptor-mediated endocytosis and autophagy with apoptosis].
- Author
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He CG, Piao YJ, and Hu LM
- Subjects
- Animals, Female, Male, Mice, Microscopy, Electron, Scanning, Apoptosis, Autophagy, Endocytosis, Macrophages, Peritoneal ultrastructure, Receptors, Cell Surface physiology
- Abstract
Objective: To evaluate the relationship between receptor-mediated endocytosis, autophagosome formation and apoptosis by observing the morphological changes of mouse peritoneal macrophages in the course of receptor-mediated endocytotic activities, autophagy and apoptosis., Methods: Mouse peritoneal macrophages were incubated with horseradish peroxidase-labeled concanavalin A (ConA-HRP), and morphological examinations were performed at different time points after the incubation., Results: After the incubation of the macrophages with ConA-HRP, ConA-HRP was observed to enter the vesicles by way of receptor-mediated endocytosis. Three kinds of endosomes were observed, namely vesicles, tubes and double-membrane sheets. The double-membrane sheets enveloped a portion of the cytoplasm and organelles, thus giving rise to vesicles, or the autophagosomes, which later fused with lysosome, followed by the apoptosis of the macrophages., Conclusion: Receptor-mediated endocytosis of ConA-HRP is associated with autophagy and apoptosis.
- Published
- 2003
3. Baicalein suppresses the proliferation of human cervical cancer cells via Notch 1/Hes signaling pathway
- Author
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Tang Xiaoping, Yuan Hui, Tang Wei, Hu Lian, Xia Jiyi, and Yu Xiaolan
- Subjects
0301 basic medicine ,baicalein ,cervical cancer ,Notch signaling pathway ,Uterine Cervical Neoplasms ,Apoptosis ,lcsh:RC254-282 ,HeLa ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Notch 3 ,Cell Line, Tumor ,Basic Helix-Loop-Helix Transcription Factors ,hairy enhancer of split-5 ,Humans ,Radiology, Nuclear Medicine and imaging ,notch 1 ,Viability assay ,Receptor, Notch1 ,Notch 2 ,Notch 1 ,Cell Proliferation ,biology ,General Medicine ,hairy enhancer of split-1 ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,biology.organism_classification ,Antineoplastic Agents, Phytogenic ,Baicalein ,Repressor Proteins ,030104 developmental biology ,Oncology ,chemistry ,Hes3 signaling axis ,030220 oncology & carcinogenesis ,Flavanones ,Cancer research ,Transcription Factor HES-1 ,Female ,Signal Transduction - Abstract
Background: Baicalein is an active compound extracted from the roots of Scutellaria baicalensis georgi, which is widely and traditionally used in the anticancer therapy. Notch signaling pathway is usually abnormally activated in kinds of human cancers. The aim of the present study is to investigate the antitumor effects of baicalein in human cervical cancer and explore whether baicalein treatment affects notch signaling pathway in human cervical cancers. Materials and Methods: Cervical cancer cells were treated with increasing concentrations of baicalein for 24, 48, and 72 h, respectively. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to determine cell viability of cervical cancer cells. The apoptosis rate was determined by FACS assay. Furthermore, the molecular mechanism was investigated. The expression levels of Notch 1, Notch 2, Notch 3, hairy enhancer of split-1 (Hes-1), and Hes-5 were determined by western blotting analysis. Results: MTT assay results revealed that baicalein inhibited cell proliferation of HeLa cells and SiHa cells in a time- and dose-dependent manner. The data from FACS assay demonstrated that baicalein-induced cell apoptosis of cervical cancer cells at the final concentration of 100 μM for 24 h. Furthermore, baicalein treatment downregulated Notch 1/Hes-1, Hes-5 signaling pathway, and there was no obvious change on the expression of Notch 2 and Notch 3. Conclusion: Baicalein inhibited the proliferation of human cervical cancer cells via Notch 1/Hes signaling Pathway. The study would provide some new clues in the clinical therapy of human cervical cancers.
- Published
- 2019
4. Long non-coding RNA HAND2-AS1/miR-106a/PTEN axis re-sensitizes cisplatin-resistant ovarian cells to cisplatin treatment.
- Author
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Li, Lijun, Li, Li, Hu, Lian, Li, Ting, Xie, Dan, and Liu, Xiaoliu
- Subjects
LINCRNA ,CISPLATIN ,GENE expression ,PI3K/AKT pathway ,PTEN protein ,APOPTOSIS - Abstract
Cisplatin (DDP) resistance in patients suffering from ovarian cancer is a considerable hurdle to successful treatment. The present study aimed to identify a possible long non-coding RNA (lncRNA)-microRNA (miRNA)-mRNA axis participating in ovarian cancer DDP-resistance based on the critical roles of non-coding RNAs, including lncRNAs and miRNAs, in carcinogenesis. According to online data and experimental results, lncRNA HAND2-AS1 expression was significantly downregulated within ovarian carcinoma, especially within recurrent and DDP-resistant ovarian carcinoma. The expression of HAND2-AS1 was also shown to be markedly inhibited in SKOV3/DDP (DDP) cells with resistance to DDP. In SKOV3/DDP cells, HAND2-AS1 overexpression inhibited cell viability and promoted cell apoptosis upon DDP treatment through the Bcl-2/caspase-3 apoptotic signaling. It was hypothesized that PTEN mRNA expression was also markedly inhibited in SKOV3/DDP ovarian cancer cells, while HAND2-AS1 overexpression rescued PTEN proteins and blocked PI3K/AKT signaling activation. Moreover, miR-106a was found to bind directly to PTEN 3′ UTR and HAND2-AS1. Upon DDP treatment, miR-106a overexpression in SKOV3/DDP cells promoted cell viability. It inhibited cell apoptosis through the Bcl-2/caspase-3 apoptotic signaling pathway and downregulated the protein levels of PTEN and upregulated PI3K/AKT signaling activity. Furthermore, miR-106a overexpression partially reversed the effect of HAND2-AS1 overexpression upon PTEN proteins and SKOV3/DDP cell proliferation upon DDP treatment. In conclusion, a lncRNA HAND2-AS1/miR-106a/PTEN axis that re-sensitizes DDP-resistant SKOV3/DDP cells to DDP treatment has been established. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
5. Exogenous leptin affects sperm parameters and impairs blood testis barrier integrity in adult male mice.
- Author
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Wang, Xiaotong, Zhang, Xiaoke, Hu, Lian, and Li, Honggang
- Subjects
PHYSIOLOGICAL effects of leptin ,MALE infertility ,SPERM motility ,SPERM count ,SERTOLI cells ,TESTOSTERONE ,APOPTOSIS ,MALE reproductive organs - Abstract
Background: Serum leptin levels are augmented in obese infertile men and in men with azoospermia. They also correlate inversely with sperm concentration, motility and normal forms. The mechanisms underlying the adverse effects of excess leptin on male reproductive function remain unclear. The present study aimed to evaluate the effects of exogenous leptin on sperm parameters in mice and to explore the underlying mechanisms. Methods: We treated normal adult male mice with saline, 0.1, 0.5 or 3 mg/kg leptin daily for 2 weeks. After treatment, serum leptin levels, serum testosterone levels, sperm parameters and testicular cell apoptosis were evaluated. Blood testis barrier integrity and the expression of tight junction-associated proteins in testes were also assessed. We further verified the direct effects of leptin on tight junction-associated proteins in Sertoli cells and the possible leptin signaling pathways involved in this process. Results: After treatment, there were no significant differences in body weights, reproductive organ weights, serum leptin levels and serum testosterone levels between leptin-treated mice and control mice. Administration of 3 mg/kg leptin reduced sperm concentration, motility and progressive motility while increasing the percentage of abnormal sperm and testicular cell apoptosis. Mice treated with 3 mg/kg leptin also had impaired blood testis barrier integrity, which was related to decreased tight junction-associated proteins in testes. Leptin directly reduced tight junction-associated proteins in Sertoli cells, JAK2/STAT, PI3K and ERK pathways were suggested to be involved in this process. Conclusions: Exogenous leptin negatively affects sperm parameters and impairs blood testis barrier integrity in mice. Leptin reduced tight junction-associated proteins in Sertoli cells, indicating that leptin has a direct role in impairing blood testis barrier integrity. Given the function of blood testis barrier in maintaining normal spermatogenesis, leptin-induced blood testis barrier impairment may be one of the mechanisms contributing to male subfertility and infertility. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
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