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Yu Y.-Q.,the Affiliated Hospital of Guilin Medical College
Asian Pacific journal of cancer prevention : APJCP | Year: 2016

BACKGROUND: MicroRNAs (miRNAs) have fundamental roles in tumorigenesis. MiR-675 is upregulated in hepatocellular carcinoma(HCC) cells. However, the roles of miR-675 in hepatocellular carcinogenesis are still not fully elucidated. In this study, we focus on investigating the effect and mechanism of miR-675 in proliferation of HCC cells.MATERIALS AND METHODS: The cell proliferation was measured by MTT assays after transfection with miR-675 inhibitor and miR-675 mimics in HCC cells. The expression level of miR-675 was detected by real-time quantitative reverse transcription polymerase chain reaction. Protein expression of Cdc25A was measured by western blotting analysis.RESULTS: In MTT assays, overexpression of miR-675 promoted the proliferation of HCC cells(<0.05. at 48 hours, <0.01. at 72 hours) compared with the miR-675mimics control group. Downexpression of miR-675 inhibited the proliferation of HCC cells(<0.05. at 48 hours, <0.01. at 72 hours) compared with the miR-675inhibitor control group. In western blotting analysis, the expression level of Cdc25A was significantly increased (<0.05) after treatment with miR-675 mimics. The expression level of Cdc25A was significantly decreased (<0.05) after treatment with miR-675 inhibitor.CONCLUSIONS: Our results indicate that miR-675 promotes proliferation in human hepatocellular carcinoma cells by associating with the Cdc25A signaling pathway.


PubMed | The Affiliated Hospital of Guilin Medical College, Guangxi Zhuang Autonomous Region Center for Disease Control and Prevention, Guangxi Medical University and Guilin Medical College
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

The p53 tumor suppressor and its negative regulator, murine double minute 2 (MDM2), play critical roles in carcinogenesis. P53 codon 72 and MDM2 309T>G polymorphisms could influence p53 and MDM2 function, respectively, and might affect cancer susceptibility. We therefore investigated the association between these two SNPs, alone or in combination, and the risk of hepatocellular carcinoma (HCC) in Chinese. In this case-control study, we genotyped p53 codon 72 and MDM2 309T>G polymorphisms in 985 HCC cases and 992 cancer-free age- and sex-matched controls and evaluated their associations with the risk of HCC. Although no significant main effects were found for these two SNPs in the single-locus analysis and stratified analysis by age, sex, smoking, drinking, and hepatitis B virus (HBV) infection, we found that individuals carrying at least one G allele of the MDM2 309T>G polymorphism had statistically significant increased risk of HCC among those with the p53 Pro/Pro genotype (adjusted odds ratio (OR)=2.23, 95% confidence interval (95%CI)=1.20-4.14 for TG genotype; adjusted OR=2.67, 95%CI=1.32-5.42 for GG genotype), and the interaction between p53 codon 72 and MDM2 309T>G was significant (P interaction=0.017). Our findings suggest that the interaction of p53 codon 72 and MDM2 309T>G may play an important role in the etiology of HCC. More studies with well-designed and large sample sizes are required to validate these observations.


PubMed | Renmin University of China, the Affiliated Hospital of Guilin Medical College and Wuhan University
Type: Journal Article | Journal: PloS one | Year: 2015

To examine the hypothesis that hydrogen sulfide (H2S) regulates the colonic motility by modulating both L-type voltage-dependent calcium channels and large conductance Ca2+-activated K+ (BKCa) channels.Immunohistochemistry was performed on rat colonic samples to investigate the localization of the H2S-producing enzymes cystathionine--synthase (CBS) and cystathionine--lyase (CSE). The contractions of proximal colonic smooth muscle were studied in an organ bath system. The whole-cell patch-clamp technique was used to record both L-type calcium currents (ICa,L) and BKCa currents in colonic smooth muscle cells (SMCs) isolated from male Wistar rats.Immunohistochemistry revealed the presence of CBS and CSE in mucosa, smooth muscle cells and myenteric neurons. The H2S donor NaHS inhibited spontaneous contractions of the longitudinal muscle and circular muscle strips in a dose-dependent manner, and the inhibitory effects were not blocked by tetrodotoxin. NaHS inhibited the peak ICa,L in colonic SMCs at a membrane potential of 0 mV. The current-voltage (I-V) relationship of L-type calcium channels was modified by NaHS, and the peak of the I-V curve was shifted to the right. NaHS (200 ) evoked a significant rightward shift of the steady-state activation curve and inhibited the inactivation of L-type calcium channels. Furthermore, NaHS reversibly decreased the peak ICa,L in a dose-dependent manner. Likewise, BKCa channels were significantly inhibited by NaHS, and the addition of NaHS caused a time- and dose-dependent reduction in the BKCa current.The relaxant effect of H2S on colonic muscle strips may be associated with the direct inhibition of H2S on L-type calcium channels. H2S may be involved in the regulation of calcium homeostasis in colonic SMCs of rat colon.


PubMed | the Affiliated Hospital of Guilin Medical College and Wuhan University
Type: Journal Article | Journal: Sheng li xue bao : [Acta physiologica Sinica] | Year: 2015

The present study was designed to investigate the potential role of endogenous hydrogen sulfide (H2S) in chronic stress-induced colonic hypermotility. Male Wistar rats were submitted daily to 1 h of water avoidance stress (WAS) or sham WAS (SWAS) for 10 consecutive days. The total number of fecal pellets was counted at the end of each 1 h of WAS or SWAS session. Organ bath recordings were used to test the colonic motility. HS production of colon was determined, and immunohistochemistry and Western blot were performed on rat colonic samples to detect the distribution and expression of HS-producing enzymes. The results showed that i) repeated WAS increased the number of fecal pellets per hour and the area under the curve (AUC) of the spontaneous contractions of colonic strips (P < 0.05), ii) repeated WAS decreased the endogenous production of HS and the expression of HS-producing enzymes in the colon devoid of mucosa and submucosa (P < 0.001), iii) cystathionine--lyase (CSE) was strongly expressed in the cytosols of the circular and longitudinal smooth muscle cells and the nucleus of the myenteric plexus neurons, iv) cystathionine--synthase (CBS) was primarily localized in the cytosols of myenteric plexus neurons and weakly localized in the epithelial cells and v) inhibitors of HS-producing enzymes increased the contractile activity of colonic strips in the SWAS rats (P < 0.001). In conclusion, the results suggest that the colonic hypermotility induced by repeated WAS may be associated with the decreased production of endogenous H2S.


Zhang H.,The General Hospital of Jinan Military Region | Li X.,The General Hospital of Jinan Military Region | Qian Z.,The Affiliated Hospital of Guilin Medical College
International Journal of Clinical and Experimental Medicine | Year: 2015

Objective: This study aims to investigate the characteristics of liver X receptor α (LXRα) and its target gene expression, as well as cholesterol efflux in human macrophages treated by nicotine. Methods: Human monocyte-derived macrophages were collected. Before apoA-I-mediated human monocyte-derived macrophage cholesterol efflux, and mRNA expression of LXRα, and some of its target genes being detected, the macrophages were induced with or without nicotine. Results: Pre-incubation of Human monocyte-derived macrophages with nicotine, cholesterol efflux was suppressed to apolipoprotein AI. Nicotine also inhibited LXRαand some of its target genes mRNA expression involved cholesterol metabolism, and facilitated some inflammatory genes expression. Conclusion: The changed function of cholesterol efflux and some genes expression may be the pathogenetic cause, and LXR activity of macrophage may offer potential therapeutic benefit in the treatment of atherosclerosis. Thus nicotine can regulate foam cell formation by inhibiting LXR pathway. © 2015, E-Century Publishing Corporation. All rights reserved.


Lin Z.,The Affiliated Hospital of Guilin Medical College | Liu Y.,The Affiliated Hospital of Guilin Medical College | Zheng Q.,The Affiliated Hospital of Guilin Medical College | Hu Q.,The Affiliated Hospital of Guilin Medical College
BMC Gastroenterology | Year: 2011

Background: Severe acute pancreatitis (SAP) remains a potentially life-threatening disease. Gastrointestinal motility disturbance such as intestinal ileus is seen in every case. By now, the mechanisms of pancreatitis-induced ileus are largely unknown. The main purpose of the present study was to observe changes of nitric oxide synthase-immunoreactive (NOS-IR) neurons in ileal myenteric ganglia in SAP rats with gastrointestinal dysmotility, trying to explore underlying nervous mechanisms of pancreatitis-induced ileus.Methods: Twenty Sprague Dawley rats were randomly divided into sham operated group and SAP group. SAP was induced by retrograde cholangiopancreatic duct injection of 5% sodium taurocholate. Abdominal X-ray and intestinal transit were performed to detect the existence of paralytic ileus and intestinal dysmotility. Pathological damage of pancreas was evaluated. Double-immunolabeling was employed for the whole-mount preparations of ileal myenteric ganglia. The morphology of NOS-IR neurons were observed and the percentage of NOS-IR neurons was calculated based on the total Hu-immunoreactive neurons. Total RNA of ileum was extracted according to Trizol reagent protocol. Neuronal NOS (nNOS) mRNA expression was evaluated by RT-PCR.Results: The small intestinal transit index in the SAP group was significantly lower compared with the sham operated group (29.21 ± 3.68% vs 52.48 ± 6.76%, P < 0.01). The percentage of NOS-IR neurons in ileal myenteric ganglia in the SAP group was significantly higher than that in the sham operated group (37.5 ± 12.28% vs 26.32 ± 16.15%, P < 0.01). nNOS mRNA expression in ileum of SAP group was significantly higher than that in the sham operated group (1.02 ± 0.10 vs 0.70 ± 0.06, P < 0.01).Conclusions: The increased quantity of NOS-IR neurons in ileal myenteric ganglia and increased nNOS mRNA expression may suggest nNOS over expression as one of the nervous mechanisms of gastrointestinal dysmotility in SAP rat. © 2011 Lin et al; licensee BioMed Central Ltd.


Mo H.Y.,the Affiliated Hospital of Guilin Medical College
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases | Year: 2011

To investigate the mechanisms of cyclophosphamide sequential therapy for patients with primary Sjögren's syndrome-associated interstitial lung disease (PSS-ILD). This was a retrospective review of 15 patients (2005 - 2008) with PSS-ILD who underwent cyclophosphamide sequential therapy. Peripheral blood and bronchoalveolar lavage (BALF) were obtain before and 3, 6, 12, 24 months after the treatment. The TNF-α and TGF-β(1)mRNA levels in peripheral blood were measured using reverse transcription-polymerase chain reaction (RT-PCR). Serum and BALF TNF-α, TGF-β(1)and MMP-9 levels were measured using sandwich enzyme-linked immunosorbent assay (ELISA). (1) The average levels of serum TNF-α (0.39 ± 0.22) and TGF-β(1) (0.31 ± 0.18) mRNA in patients with PSS-ILD were higher compared with that in patients with PSS without ILD. TNF-α level (0.23 ± 0.19) was significantly decreased 3 months after cyclophosphamide treatment (t = 2.533, P < 0.05), and TGF-β(1) (0.31 ± 0.18) level markedly decreased after 6 months of treatment (t = 2.617, P < 0.05). (2) The levels of serum TNF-α (11.2 ± 2.6) μg/L, TGF-β(1) (72 ± 19) μg/L and MMP-9 (38 ± 9) μg/L in patients with PSS-ILD were higher than that in patients with PSS without ILD. TGF-β(1) (36 ± 12) μg/L level decreased significantly after 3 months of treatment (t = 2.526, P < 0.05), and TNF-α level (7.1 ± 1.3) μg/L markedly decreased after 6 months of therapy (t = 2.578, P < 0.05). MMP-9 level (18 ± 4) μg/L decreased significantly after 12-month treatment (t = 2.329, P < 0.05). (3) The levels of BALF TNF-α (17.1 ± 3.5) μg/L, TGF-β(1) (36 ± 17) μg/L and MMP-9 (27 ± 10) μg/L in patients with PSS-ILD were higher than that in patients with PSS without ILD. TGF-β(1) (21 ± 14) μg/L level decreased significantly after 3-month treatment, and TNF-α level (9.4 ± 1.7) μg/L was decreased after 6 months of cyclophosphamide treatment (t = 2.215, P < 0.05). MMP-9 level (13 ± 5) μg/L decreased after 12 months of cyclophosphamide treatment (t = 2.576, P < 0.05). The mechanisms of cyclophosphamide treatment may be associated with its inhibition on production of TNF-α, TGF-β(1)and MMP-9.


Zhao C.,the Affiliated Hospital of Guilin Medical College
Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery | Year: 2012

To discuss the effect of reducing the cricopharyngeal dysfunction on the Groningen prosthesis voice restoration following total laryngectomy and the effect of different methods. Fifty-six patients were implanted with Groningen voice prostheses to rebuild voice after total laryngectomy. The clinical data were analyzed retrospectively. Of 56 patients, 412 patients successes in voice restoration. The success rate of amputating pharynx plexus nerves group was 60.0%, amputating cricopharyngeal muscle group was 62.5%, and the amputating pharynx plexus nerves and cricopharyngeal muscle group was 96.0%. The combination of pharynx plexus nerves resection and cricopharyngeal myotomy can make higher success rate of voice restoration.


PubMed | The Affiliated Hospital of Guilin Medical College and Central South University
Type: | Journal: Stem cells international | Year: 2016

Leukemia stem cells (LSCs) play the major role in relapse of acute myeloid leukemia (AML). Recent evidence indicates that microvesicles (MVs) released from cancer stem cells can promote tumor growth and invasion. In this study, we investigated whether LSCs-released MVs (LMVs) can regulate the malignance of AML cells and whether overexpression of tumor suppressive microRNA (miR), miR34a, is able to interrupt this process. LSCs were transfected with miRNA control (miRCtrl) or miR34a mimic for producing LMVs, respectively, defined as LMVs(miRCtrl) and LMVs(miR34a). The effect of miR34a transfection on LSC proliferation and the effects of LMVs(miRCtrl) or LMVs(miR34a) on the proliferation, migration, and apoptosis of AML cells (after LSC depletion) were determined. The levels of miR34a targets, caspase-3 and T cell immunoglobulin mucin-3 (Tim-3), were analyzed. Results showed that (1) LMVs(miRCtrl) promoted proliferation and migration and inhibited apoptosis of AML cells, which were associated with miR34a deficit; (2) transfection of miR34a mimic inhibited LSC proliferation and increased miR34a level in LMVs(miR34a); (3) LMVs(miR34a) produced opposite effects as compared with LMVs(miRCtrl), which were associated with the changes of caspase-3 and Tim-3 levels. In summary, LMVs support AML cell malignance and modulating miR34a could offer a new approach for the management of AML.


PubMed | the Affiliated Hospital of Guilin Medical College
Type: Journal Article | Journal: Asian Pacific journal of cancer prevention : APJCP | Year: 2016

MicroRNAs (miRNAs) have fundamental roles in tumorigenesis. MiR-675 is upregulated in hepatocellular carcinoma(HCC) cells. However, the roles of miR-675 in hepatocellular carcinogenesis are still not fully elucidated. In this study, we focus on investigating the effect and mechanism of miR-675 in proliferation of HCC cells.The cell proliferation was measured by MTT assays after transfection with miR-675 inhibitor and miR-675 mimics in HCC cells. The expression level of miR-675 was detected by real-time quantitative reverse transcription polymerase chain reaction. Protein expression of Cdc25A was measured by western blotting analysis.In MTT assays, overexpression of miR-675 promoted the proliferation of HCC cells(<0.05. at 48 hours, <0.01. at 72 hours) compared with the miR-675mimics control group. Downexpression of miR-675 inhibited the proliferation of HCC cells(<0.05. at 48 hours, <0.01. at 72 hours) compared with the miR-675inhibitor control group. In western blotting analysis, the expression level of Cdc25A was significantly increased (<0.05) after treatment with miR-675 mimics. The expression level of Cdc25A was significantly decreased (<0.05) after treatment with miR-675 inhibitor.Our results indicate that miR-675 promotes proliferation in human hepatocellular carcinoma cells by associating with the Cdc25A signaling pathway.

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